murine pc pan02 cell line  (ATCC)


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    Structured Review

    ATCC murine pc pan02 cell line
    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of <t>PAN02</t> cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
    Murine Pc Pan02 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/murine pc pan02 cell line/product/ATCC
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    murine pc pan02 cell line - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses"

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    Journal: Nature Communications

    doi: 10.1038/s41467-024-49825-6

    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
    Figure Legend Snippet: a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.

    Techniques Used: In Situ, Labeling, Fluorescence, Membrane

    a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.

    Techniques Used: Fluorescence, Injection, Ex Vivo

    a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.

    Techniques Used: Two Tailed Test, Flow Cytometry

    mice pan02 pancreatic cancer cell lines  (ATCC)


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    Structured Review

    ATCC mice pan02 pancreatic cancer cell lines
    Mice Pan02 Pancreatic Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mice pan02 pancreatic cancer cell lines/product/ATCC
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mice pan02 pancreatic cancer cell lines - by Bioz Stars, 2024-07
    86/100 stars

    Images


    Structured Review

    Revvity Signals pan02 tumor bearing mice
    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of <t>PAN02</t> cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
    Pan02 Tumor Bearing Mice, supplied by Revvity Signals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pan02 tumor bearing mice/product/Revvity Signals
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pan02 tumor bearing mice - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses"

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    Journal: Nature Communications

    doi: 10.1038/s41467-024-49825-6

    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
    Figure Legend Snippet: a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.

    Techniques Used: In Situ, Labeling, Fluorescence, Membrane

    a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.

    Techniques Used: Fluorescence, Injection, Ex Vivo

    a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.

    Techniques Used: Two Tailed Test, Flow Cytometry


    Structured Review

    Charles River Laboratories pan02 mouse male cells
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Pan02 Mouse Male Cells, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer"

    Article Title: Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms25137438

    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine Pan02 allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Figure Legend Snippet: GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine Pan02 allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Techniques Used: RNA Expression, Expressing, Generated, Western Blot, Cell Culture, Real-time Polymerase Chain Reaction, Immunocytochemistry, Staining, Saline, Recombinant, Injection, Transgenic Assay, Comparison

    GH upregulates ABC multidrug transporter expression in PDAC: ( A ) List of top 15 (false detection rate <0.05) ABC transporter expression correlations with GHR expression in 171 human PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of ABC transporters following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) (top) Cellular drug efflux rate and (bottom) cellular retention of fluorescent DiOC2 (ABC transporter substrate) in pancreatic cancer cells treated with either GH, GH + pegvisomant, or GH + compound G. ( D ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels showing fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( E – H ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of ABC transporters in ( E ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( F ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( G ) PANC1 tumors in female nude mice treated with compound-G–gemcitabine combination, or ( H ) Pan02 tumors from bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Figure Legend Snippet: GH upregulates ABC multidrug transporter expression in PDAC: ( A ) List of top 15 (false detection rate <0.05) ABC transporter expression correlations with GHR expression in 171 human PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of ABC transporters following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) (top) Cellular drug efflux rate and (bottom) cellular retention of fluorescent DiOC2 (ABC transporter substrate) in pancreatic cancer cells treated with either GH, GH + pegvisomant, or GH + compound G. ( D ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels showing fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( E – H ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of ABC transporters in ( E ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( F ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( G ) PANC1 tumors in female nude mice treated with compound-G–gemcitabine combination, or ( H ) Pan02 tumors from bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Techniques Used: Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Comparison

    GH induces expression of epithelial-to-mesenchymal transition (EMT) factors in PDAC: ( A ) List of Pearson correlation coefficients of top 15 EMT-related genes (false detection rate < 0.05) with GHR expression in human 171 PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of EMT factors following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) Effects of treatment with either GH, GH + pegvisomant, or GH + compound G on basement membrane invasion capacity of pancreatic cancer cells in culture. ( D ) Number of viable colonies formed by human and mouse pancreatic cancer cells following treatment with either GH, GH + pegvisomant, or GH + compound G in the presence/absence of chemotherapy (doxorubicin or gemcitabine). ( E ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels and fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( F – I ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of EMT factors in ( F ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( G ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( H ) PANC1 tumors in female nude mice treated with compound G–gemcitabine combination, or ( I ) Pan02 tumors from male bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Figure Legend Snippet: GH induces expression of epithelial-to-mesenchymal transition (EMT) factors in PDAC: ( A ) List of Pearson correlation coefficients of top 15 EMT-related genes (false detection rate < 0.05) with GHR expression in human 171 PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of EMT factors following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) Effects of treatment with either GH, GH + pegvisomant, or GH + compound G on basement membrane invasion capacity of pancreatic cancer cells in culture. ( D ) Number of viable colonies formed by human and mouse pancreatic cancer cells following treatment with either GH, GH + pegvisomant, or GH + compound G in the presence/absence of chemotherapy (doxorubicin or gemcitabine). ( E ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels and fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( F – I ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of EMT factors in ( F ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( G ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( H ) PANC1 tumors in female nude mice treated with compound G–gemcitabine combination, or ( I ) Pan02 tumors from male bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Techniques Used: Expressing, Western Blot, Membrane, Reverse Transcription, Real-time Polymerase Chain Reaction, Comparison

    GH-induced gene expression has a multi-modal therapy refractory signature in PDAC: ( A – F ) List of marker genes most significantly (Pearson coefficient > 0.3, false detection rate (FDR) < 0.05) correlated with GHR expression in human PDAC patients, associated with the therapy-resistant processes (modules) of fibrosis ( A ), apoptosis ( B ), angiogenesis ( C ), lymphangiogenesis ( D ), senescence ( E ), stemness ( F ), and cytochrome P450s ( G ). ( H ) Heatmap depicting RT-qPCR cross-validation of RNA expression pattern of selected genes from each module (in ( A – G )) in Pan02 tumors from WT vs. bGH male mice.
    Figure Legend Snippet: GH-induced gene expression has a multi-modal therapy refractory signature in PDAC: ( A – F ) List of marker genes most significantly (Pearson coefficient > 0.3, false detection rate (FDR) < 0.05) correlated with GHR expression in human PDAC patients, associated with the therapy-resistant processes (modules) of fibrosis ( A ), apoptosis ( B ), angiogenesis ( C ), lymphangiogenesis ( D ), senescence ( E ), stemness ( F ), and cytochrome P450s ( G ). ( H ) Heatmap depicting RT-qPCR cross-validation of RNA expression pattern of selected genes from each module (in ( A – G )) in Pan02 tumors from WT vs. bGH male mice.

    Techniques Used: Expressing, Marker, Quantitative RT-PCR, RNA Expression

    bag6 wt ko pan02 cells  (Selleck Chemicals)


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    Selleck Chemicals bag6 wt ko pan02 cells
    Bag6 Wt Ko Pan02 Cells, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology bag6 wt ko pan02 cells
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    Corning Life Sciences 106 pan02 cells
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    culturing media murine pancreatic adenocarcinoma cell line pan02  (Thermo Fisher)


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    Thermo Fisher culturing media murine pancreatic adenocarcinoma cell line pan02
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    GenTarget pan02 luc
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    pan02 luc  (Thermo Fisher)


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    ATCC murine pc pan02 cell line
    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of <t>PAN02</t> cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
    Murine Pc Pan02 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC mice pan02 pancreatic cancer cell lines
    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of <t>PAN02</t> cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
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    Revvity Signals pan02 tumor bearing mice
    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of <t>PAN02</t> cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.
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    Charles River Laboratories pan02 mouse male cells
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Pan02 Mouse Male Cells, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Selleck Chemicals bag6 wt ko pan02 cells
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Bag6 Wt Ko Pan02 Cells, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology bag6 wt ko pan02 cells
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Bag6 Wt Ko Pan02 Cells, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Corning Life Sciences 106 pan02 cells
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    106 Pan02 Cells, supplied by Corning Life Sciences, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher culturing media murine pancreatic adenocarcinoma cell line pan02
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Culturing Media Murine Pancreatic Adenocarcinoma Cell Line Pan02, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GenTarget pan02 luc
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Pan02 Luc, supplied by GenTarget, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher pan02 luc
    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine <t>Pan02</t> allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.
    Pan02 Luc, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.

    Journal: Nature Communications

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    doi: 10.1038/s41467-024-49825-6

    Figure Lengend Snippet: a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.

    Article Snippet: Murine BC 4T1 cell line, murine PC PAN02 cell line, human BC MDA-MB-231 cell line, murine macrophage cell line RAW264.7, and human macrophage cell line THP-1 were purchased from the American Type Culture Collection (ATCC) and cultured according to the supplier’s recommendations, supplemented with 10% fetal bovine serum (FBS) and antibiotics.

    Techniques: In Situ, Labeling, Fluorescence, Membrane

    a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    doi: 10.1038/s41467-024-49825-6

    Figure Lengend Snippet: a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.

    Article Snippet: Murine BC 4T1 cell line, murine PC PAN02 cell line, human BC MDA-MB-231 cell line, murine macrophage cell line RAW264.7, and human macrophage cell line THP-1 were purchased from the American Type Culture Collection (ATCC) and cultured according to the supplier’s recommendations, supplemented with 10% fetal bovine serum (FBS) and antibiotics.

    Techniques: Fluorescence, Injection, Ex Vivo

    a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    doi: 10.1038/s41467-024-49825-6

    Figure Lengend Snippet: a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.

    Article Snippet: Murine BC 4T1 cell line, murine PC PAN02 cell line, human BC MDA-MB-231 cell line, murine macrophage cell line RAW264.7, and human macrophage cell line THP-1 were purchased from the American Type Culture Collection (ATCC) and cultured according to the supplier’s recommendations, supplemented with 10% fetal bovine serum (FBS) and antibiotics.

    Techniques: Two Tailed Test, Flow Cytometry

    a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.

    Journal: Nature Communications

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    doi: 10.1038/s41467-024-49825-6

    Figure Lengend Snippet: a Schematic illustration of tumor immune quiescent microenvironment, in situ assembly of PAC-SABIs on the cancer cell surface, and blockage of CD47 and CD24 phagocytic checkpoints by PAC-SABIs. Figure was created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. b Time-dependent CLSM images of 4T1 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. c Time-dependent CLSM images of PAN02 cells treated with NBD-labeled PAC-SABIs. Scale bar: 20 μm. Three independent experiments were performed. d Merged bright field and fluorescence images of 4T1 cell treated with NBD-labeled PAC-SABIs for 120 min. Scale bar: 20 μm. Three independent experiments were performed. e CLSM images of 4T1 cell treated with Dil dye (red) and NBD-labeled PAC-SABIs for 120 min. Scale bar: 10 μm. Three independent experiments were performed. f , g Fluorescence distribution of NBD-labeled PAC-SABIs on 4T1 cell. Three independent experiments were performed. h Time-dependent SEM images of 4T1 cells treated with PAC-SABIs. The red arrows point to PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. i Time-dependent SEM images of PAN02 cells treated with PAC-SABIs. The red arrows point to the PAC-SABIs on cell membrane. Scale bar: 2 μm. Three independent experiments were performed. j CLSM images of 3D 4T1 spheroids treated with Cy5.5 PAC-SABIs, Calcein-AM, and Hoechst 33342. Scale bar: 50 μm. Three independent experiments were performed. k CLSM images of 3D 4T1 spheroids along the z -axis position. Scale bar: 50 μm. Three independent experiments were performed.

    Article Snippet: The 4T1 and PAN02 tumor-bearing mice were correspondingly intravenously injected with free Cy5.5, Cy5.5 SAMIs, and Cy5.5 PAC-SABIs (the dose of Cy5.5 was 1 mg/kg) for in vivo fluorescence imaging with IVIS system (Perkin Elmer, USA).

    Techniques: In Situ, Labeling, Fluorescence, Membrane

    a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    doi: 10.1038/s41467-024-49825-6

    Figure Lengend Snippet: a Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on 4T1 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The white dashed circles refer to the tumor site. b Time-dependent quantitative calculation of the average fluorescence intensity in 4T1 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). c Representative NIR fluorescence images of free Cy5.5, Cy5.5 SAMIs and Cy5.5 PAC-SABIs on PAN02 subcutaneous tumor-bearing mice after intravenous injection. Images were acquired at 0, 2, 6, 12, 24, 48, 72, 96 and 120 h post injection. The black dashed circles refer to the tumor site. d Time-dependent quantitative calculation of the average fluorescence intensity in PAN02 tumor area and AUCs of Cy5.5 SAMIs and Cy5.5 PAC-SABIs. The error bars represent the mean ± SD ( n = 3 mice). e Ex vivo NIR fluorescence images of 4T1 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. f Ex vivo NIR fluorescence images of PAN02 tumor and major organs (H heart, Li liver, S spleen, Lu lung, K kidney) collected post 48 h injection. Three independent experiments were performed. g Fluorescence images of 4T1 and PAN02 subcutaneous tumor sections at 48 h post-injection of Cy5.5 PAC-SABIs. A refers to the area of fibroids; B refers to the area of cancer cells; C refers to the paracancerous area. Scale bar: 100 μm. Three independent experiments were performed. Source data are provided as a Source Data file.

    Article Snippet: The 4T1 and PAN02 tumor-bearing mice were correspondingly intravenously injected with free Cy5.5, Cy5.5 SAMIs, and Cy5.5 PAC-SABIs (the dose of Cy5.5 was 1 mg/kg) for in vivo fluorescence imaging with IVIS system (Perkin Elmer, USA).

    Techniques: Fluorescence, Injection, Ex Vivo

    a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses

    doi: 10.1038/s41467-024-49825-6

    Figure Lengend Snippet: a Scheme of the PAC-SABIs therapeutic strategy for 4T1 orthotopic tumor. b BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). c Quantification analysis of 4T1 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; ** p < 0.01, *** p < 0.001, **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). d Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). e Scheme of the PAC-SABIs therapeutic strategy for PAN02 orthotopic tumor. f BLIs of PAN02 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). g Quantification analysis of PAN02 tumor BLI signals in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, *** p < 0.001; the p value was analyzed by a two-tailed unpaired Student’s t test). h Kaplan–Meier survival curves of PAN02 tumor-bearing mice ( n = 5 mice; * p < 0.05; the p value was analyzed by log-rank test). i Scheme of macrophage depletion and therapeutic strategy for 4T1 subcutaneous tumor. j Representative flow cytometry plots of tissue-resident macrophages. k Quantification analysis of tissue-resident macrophages. Boxplots represent the median and interquartile range, and the whiskers denote minimum and maximum values ( n = 4 mice; **** p < 0.0001; the p value was analyzed by a two-tailed unpaired Student’s t test). l BLIs of 4T1 tumor-bearing mice on days 7, 14, 21, and 28 ( n = 5 mice). m Quantification analysis of BLI signals of 4T1 tumor in each treatment group. The error bars represent the mean ± SD ( n = 5 mice; * p < 0.05, ** p < 0.01; the p value was analyzed by a two-tailed unpaired Student’s t test). n Kaplan–Meier survival curves of 4T1 tumor-bearing mice ( n = 5 mice; ** p < 0.01; the p value was analyzed by log-rank test). a , e , i were created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 international license. Source data are provided as a Source Data file.

    Article Snippet: The 4T1 and PAN02 tumor-bearing mice were correspondingly intravenously injected with free Cy5.5, Cy5.5 SAMIs, and Cy5.5 PAC-SABIs (the dose of Cy5.5 was 1 mg/kg) for in vivo fluorescence imaging with IVIS system (Perkin Elmer, USA).

    Techniques: Two Tailed Test, Flow Cytometry

    GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine Pan02 allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Journal: International Journal of Molecular Sciences

    Article Title: Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer

    doi: 10.3390/ijms25137438

    Figure Lengend Snippet: GH action is a driver of pancreatic cancer progression and inversely correlates with disease-free survival in human PDAC patients. ( A , B ) Kaplan–Meier survival plot depicting correlation of human GHR ( A ) or PRLR ( B ) RNA expression with disease-free survival in human pancreatic ductal adenocarcinoma patients [data re-analyzed using KMplotter from Posta and Gyorffy, Clinical and Translational Science , 2023, doi: 10.1111/cts.13563]. ( C ) Spearman correlation of GHR expression vs. IGF1 ( left ) and IGF2 ( right ) expression in pancreatic tumor and normal pancreatic tissue in PDAC patients (TCGA and GTEx) [data generated using GEPIA2 portal]. ( D ) ( top ) Western blot (representative blots) showing protein expression of GH and GHR in cultured pancreatic cancer cell lysates, and ( bottom ) the mean threshold cycle (Ct; higher Ct means lower expression ) values from quantitative PCR showing relative RNA expression of GH1, GHR, IGF1, IGF1R, and PRLR in pancreatic cancer cultured cells. ( E ) Immunocytochemistry for GHR (green) in cultured pancreatic cancer cells with nuclei stained with DAPI (cells in grayscale) (magnification = 20X, scale bar = 100um). ( F ) Western blot of GH downstream intracellular signaling mediators—STAT5, STAT3, SRC, AKT, and ERK1/2—in cultured pancreatic cancer cells treated with either of saline, GH (50 ng/mL), GH (50 ng/mL) + pegvisomant (500 nM), or GH (50 ng/mL) + compound G (500 nM). ( G ) Effects of 96 h treatment with the above concentrations of GH and GHR antagonists (pegvisomant and compound G) on pancreatic cancer cell growth in culture. For the above, significant differences were compared using two-way ANOVA with Tukey’s multiple comparisons test and * signifies p < 0.05. ( H ) Increases in tumor volume and final tumor weight in male nude mice (n = 4) treated with 25, 50, or 125 ug/day of recombinant human GH by intraperitoneal (i.p.) injection. ( I , J ) Effects of treatment with GHR antagonists (pegvisomant or compound G) on PANC1 xenograft tumor volume growth in male ( I ) and female ( J ) nude mice (n = 6). ( K ) Increase in murine Pan02 allograft tumor volume with time and final tumor weight in male syngeneic C57BL6 mice—wild-type (Wt) or transgenic for bovine GH (bGH; high GH, high IGF1) (n = 4). Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Article Snippet: Cell culture and treatments: Pancreatic cancer cell lines PANC1 (human male, CRL-1469), BxPC3 (human female, CRL-1687), and LTPA (mouse female, CRL-2389) were purchased from ATCC (Manassas, VA, USA), and Pan02 (mouse male) cells were obtained from Charles River (Wilmington, MA, USA).

    Techniques: RNA Expression, Expressing, Generated, Western Blot, Cell Culture, Real-time Polymerase Chain Reaction, Immunocytochemistry, Staining, Saline, Recombinant, Injection, Transgenic Assay, Comparison

    GH upregulates ABC multidrug transporter expression in PDAC: ( A ) List of top 15 (false detection rate <0.05) ABC transporter expression correlations with GHR expression in 171 human PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of ABC transporters following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) (top) Cellular drug efflux rate and (bottom) cellular retention of fluorescent DiOC2 (ABC transporter substrate) in pancreatic cancer cells treated with either GH, GH + pegvisomant, or GH + compound G. ( D ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels showing fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( E – H ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of ABC transporters in ( E ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( F ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( G ) PANC1 tumors in female nude mice treated with compound-G–gemcitabine combination, or ( H ) Pan02 tumors from bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Journal: International Journal of Molecular Sciences

    Article Title: Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer

    doi: 10.3390/ijms25137438

    Figure Lengend Snippet: GH upregulates ABC multidrug transporter expression in PDAC: ( A ) List of top 15 (false detection rate <0.05) ABC transporter expression correlations with GHR expression in 171 human PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of ABC transporters following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) (top) Cellular drug efflux rate and (bottom) cellular retention of fluorescent DiOC2 (ABC transporter substrate) in pancreatic cancer cells treated with either GH, GH + pegvisomant, or GH + compound G. ( D ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels showing fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( E – H ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of ABC transporters in ( E ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( F ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( G ) PANC1 tumors in female nude mice treated with compound-G–gemcitabine combination, or ( H ) Pan02 tumors from bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Article Snippet: Cell culture and treatments: Pancreatic cancer cell lines PANC1 (human male, CRL-1469), BxPC3 (human female, CRL-1687), and LTPA (mouse female, CRL-2389) were purchased from ATCC (Manassas, VA, USA), and Pan02 (mouse male) cells were obtained from Charles River (Wilmington, MA, USA).

    Techniques: Expressing, Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Comparison

    GH induces expression of epithelial-to-mesenchymal transition (EMT) factors in PDAC: ( A ) List of Pearson correlation coefficients of top 15 EMT-related genes (false detection rate < 0.05) with GHR expression in human 171 PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of EMT factors following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) Effects of treatment with either GH, GH + pegvisomant, or GH + compound G on basement membrane invasion capacity of pancreatic cancer cells in culture. ( D ) Number of viable colonies formed by human and mouse pancreatic cancer cells following treatment with either GH, GH + pegvisomant, or GH + compound G in the presence/absence of chemotherapy (doxorubicin or gemcitabine). ( E ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels and fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( F – I ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of EMT factors in ( F ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( G ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( H ) PANC1 tumors in female nude mice treated with compound G–gemcitabine combination, or ( I ) Pan02 tumors from male bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Journal: International Journal of Molecular Sciences

    Article Title: Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer

    doi: 10.3390/ijms25137438

    Figure Lengend Snippet: GH induces expression of epithelial-to-mesenchymal transition (EMT) factors in PDAC: ( A ) List of Pearson correlation coefficients of top 15 EMT-related genes (false detection rate < 0.05) with GHR expression in human 171 PDAC patients (TCGA database). ( B ) Western blots (representative blots and densitometric analysis) showing changes in protein levels of EMT factors following treatment with either GH, GH + pegvisomant, or GH + compound G across all four pancreatic cancer cell lines. ( C ) Effects of treatment with either GH, GH + pegvisomant, or GH + compound G on basement membrane invasion capacity of pancreatic cancer cells in culture. ( D ) Number of viable colonies formed by human and mouse pancreatic cancer cells following treatment with either GH, GH + pegvisomant, or GH + compound G in the presence/absence of chemotherapy (doxorubicin or gemcitabine). ( E ) Reverse transcription and real-time quantitative PCR of RNA from xenograft tumors for relative RNA levels and fold-changes in xenograft tumors in bGH vs. WT, and male and female nude mice with PANC1 tumors and treated with gemcitabine or GHRAs alone or in combination. ( F – I ) Western blots (representative blots and densitometric analysis) showing changes in tumor protein levels of EMT factors in ( F ) PANC1 tumors in male nude mice treated with pegvisomant–gemcitabine combination, ( G ) PANC1 tumors in male nude mice treated with compound G–gemcitabine combination, ( H ) PANC1 tumors in female nude mice treated with compound G–gemcitabine combination, or ( I ) Pan02 tumors from male bGH and Wt mice. Significant differences were compared using repeated measures ANOVA combined with Bonferroni’s multiple comparison and * signifies p < 0.05.

    Article Snippet: Cell culture and treatments: Pancreatic cancer cell lines PANC1 (human male, CRL-1469), BxPC3 (human female, CRL-1687), and LTPA (mouse female, CRL-2389) were purchased from ATCC (Manassas, VA, USA), and Pan02 (mouse male) cells were obtained from Charles River (Wilmington, MA, USA).

    Techniques: Expressing, Western Blot, Membrane, Reverse Transcription, Real-time Polymerase Chain Reaction, Comparison

    GH-induced gene expression has a multi-modal therapy refractory signature in PDAC: ( A – F ) List of marker genes most significantly (Pearson coefficient > 0.3, false detection rate (FDR) < 0.05) correlated with GHR expression in human PDAC patients, associated with the therapy-resistant processes (modules) of fibrosis ( A ), apoptosis ( B ), angiogenesis ( C ), lymphangiogenesis ( D ), senescence ( E ), stemness ( F ), and cytochrome P450s ( G ). ( H ) Heatmap depicting RT-qPCR cross-validation of RNA expression pattern of selected genes from each module (in ( A – G )) in Pan02 tumors from WT vs. bGH male mice.

    Journal: International Journal of Molecular Sciences

    Article Title: Growth Hormone Receptor Antagonist Markedly Improves Gemcitabine Response in a Mouse Xenograft Model of Human Pancreatic Cancer

    doi: 10.3390/ijms25137438

    Figure Lengend Snippet: GH-induced gene expression has a multi-modal therapy refractory signature in PDAC: ( A – F ) List of marker genes most significantly (Pearson coefficient > 0.3, false detection rate (FDR) < 0.05) correlated with GHR expression in human PDAC patients, associated with the therapy-resistant processes (modules) of fibrosis ( A ), apoptosis ( B ), angiogenesis ( C ), lymphangiogenesis ( D ), senescence ( E ), stemness ( F ), and cytochrome P450s ( G ). ( H ) Heatmap depicting RT-qPCR cross-validation of RNA expression pattern of selected genes from each module (in ( A – G )) in Pan02 tumors from WT vs. bGH male mice.

    Article Snippet: Cell culture and treatments: Pancreatic cancer cell lines PANC1 (human male, CRL-1469), BxPC3 (human female, CRL-1687), and LTPA (mouse female, CRL-2389) were purchased from ATCC (Manassas, VA, USA), and Pan02 (mouse male) cells were obtained from Charles River (Wilmington, MA, USA).

    Techniques: Expressing, Marker, Quantitative RT-PCR, RNA Expression