panc 10 05  (ATCC)


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    ATCC panc 10 05
    Panc 10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    panc 10 05  (ATCC)


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    ATCC panc 10 05
    Panc 10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    crl 2547  (ATCC)


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    ATCC crl 2547
    H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: <t>CRL-2547,</t> CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.
    Crl 2547, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Use of H19 Gene Regulatory Sequences in DNA-Based Therapy for Pancreatic Cancer"

    Article Title: Use of H19 Gene Regulatory Sequences in DNA-Based Therapy for Pancreatic Cancer

    Journal: Journal of Oncology

    doi: 10.1155/2010/178174

    H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: CRL-2547, CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.
    Figure Legend Snippet: H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: CRL-2547, CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.

    Techniques Used: Marker, Cell Culture, Generated, Injection, Negative Control

    Heterotopic model for pancreatic cancer. (a) Average tumor volume of Luc-H19 group ( n = 8) and DTA-H19 group ( n = 7) during the experiment using CRL-1469 cells. Treatments were administrated on days 0, 3, and 6 by direct intratumoral injection after subcutaneous implantation of human pancreatic carcinoma cells in the back of nude mice. Three days after the last treatment, the animals were sacrificed. (b) Average of ex vivo tumor volume at the end of the experiment, tumors generated using CRL-1469 cells. (c) Tumor Growth Progression of Luc-H19 ( n = 5) and DTA-H19 ( n = 5) groups, in experiment using CRL-2547 cell line.
    Figure Legend Snippet: Heterotopic model for pancreatic cancer. (a) Average tumor volume of Luc-H19 group ( n = 8) and DTA-H19 group ( n = 7) during the experiment using CRL-1469 cells. Treatments were administrated on days 0, 3, and 6 by direct intratumoral injection after subcutaneous implantation of human pancreatic carcinoma cells in the back of nude mice. Three days after the last treatment, the animals were sacrificed. (b) Average of ex vivo tumor volume at the end of the experiment, tumors generated using CRL-1469 cells. (c) Tumor Growth Progression of Luc-H19 ( n = 5) and DTA-H19 ( n = 5) groups, in experiment using CRL-2547 cell line.

    Techniques Used: Injection, Ex Vivo, Generated

    panc10 05 cells  (ATCC)


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    ATCC panc10 05 cells
    Panc10 05 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    panc10 05  (ATCC)


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    ATCC panc10 05
    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and <t>Panc10.05</t> (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Panc10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    panc10 05 - by Bioz Stars, 2024-05
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    1) Product Images from "Extensive preclinical validation of combined RMC-4550 and LY3214996 supports clinical investigation for KRAS mutant pancreatic cancer"

    Article Title: Extensive preclinical validation of combined RMC-4550 and LY3214996 supports clinical investigation for KRAS mutant pancreatic cancer

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2022.100815

    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " title="... cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also Figure S1 .

    Techniques Used: Mutagenesis, Western Blot, Derivative Assay, Lysis, Colony Assay, Staining, Inhibition, Software, Concentration Assay


    Figure Legend Snippet:

    Techniques Used: Derivative Assay, Recombinant, Western Blot, Mouse Assay, Software

    panc10 05  (ATCC)


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    ATCC panc10 05
    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS <t>G12D</t> ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and <t>Panc10.05</t> (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Panc10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/panc10 05/product/ATCC
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    1) Product Images from "Extensive preclinical validation of combined RMC-4550 and LY3214996 supports clinical investigation for KRAS mutant pancreatic cancer"

    Article Title: Extensive preclinical validation of combined RMC-4550 and LY3214996 supports clinical investigation for KRAS mutant pancreatic cancer

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2022.100815

    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " title="... cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also Figure S1 .

    Techniques Used: Mutagenesis, Western Blot, Derivative Assay, Lysis, Colony Assay, Staining, Inhibition, Software, Concentration Assay


    Figure Legend Snippet:

    Techniques Used: Derivative Assay, Recombinant, Western Blot, Mouse Assay, Software

    crl  (ATCC)


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    ATCC crl
    Crl, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    panc10 05  (ATCC)


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    ATCC panc10 05
    a, SHANK3 expression (mRNA levels; the mean ± s.d) of control (siCTRL) and SHANK3 -silenced (siSHANK3_2 and siSHANK3_7 are two different siRNAs) cancer cell lines with distinct KRAS mutations (PDAC: PANC-1, <t>Panc10.05,</t> AsPC-1, Su86.86, SW1990, YAPC, PaTu8602 and MIA PaCa-2; NSCLC: A549 and H441; CRC: HCT-15 and HCT-116) or with wild-type KRAS (NSCLC: H292, H226 and H226; CRC: HT-29) and non-transformed cells (ARPE-19). b,c, Spheroid growth of control or SHANK3 -silenced KRAS -mutant AsPC-1 cells. b, SHANK3 mRNA levels. c, Representative images and quantification (mean ± s.d.) of the spheroid areas from n = 3 independent experiments. Unpaired Student’s t-test with Welch’s correction (at the endpoint). d, A schematic illustration of the chick embryo chorioallantoic membrane (CAM) xenograft assay.
    Panc10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Targeting a broad spectrum of KRAS -mutant cancers by hyperactivation-induced cell death"

    Article Title: Targeting a broad spectrum of KRAS -mutant cancers by hyperactivation-induced cell death

    Journal: bioRxiv

    doi: 10.1101/2022.09.21.508660

    a, SHANK3 expression (mRNA levels; the mean ± s.d) of control (siCTRL) and SHANK3 -silenced (siSHANK3_2 and siSHANK3_7 are two different siRNAs) cancer cell lines with distinct KRAS mutations (PDAC: PANC-1, Panc10.05, AsPC-1, Su86.86, SW1990, YAPC, PaTu8602 and MIA PaCa-2; NSCLC: A549 and H441; CRC: HCT-15 and HCT-116) or with wild-type KRAS (NSCLC: H292, H226 and H226; CRC: HT-29) and non-transformed cells (ARPE-19). b,c, Spheroid growth of control or SHANK3 -silenced KRAS -mutant AsPC-1 cells. b, SHANK3 mRNA levels. c, Representative images and quantification (mean ± s.d.) of the spheroid areas from n = 3 independent experiments. Unpaired Student’s t-test with Welch’s correction (at the endpoint). d, A schematic illustration of the chick embryo chorioallantoic membrane (CAM) xenograft assay.
    Figure Legend Snippet: a, SHANK3 expression (mRNA levels; the mean ± s.d) of control (siCTRL) and SHANK3 -silenced (siSHANK3_2 and siSHANK3_7 are two different siRNAs) cancer cell lines with distinct KRAS mutations (PDAC: PANC-1, Panc10.05, AsPC-1, Su86.86, SW1990, YAPC, PaTu8602 and MIA PaCa-2; NSCLC: A549 and H441; CRC: HCT-15 and HCT-116) or with wild-type KRAS (NSCLC: H292, H226 and H226; CRC: HT-29) and non-transformed cells (ARPE-19). b,c, Spheroid growth of control or SHANK3 -silenced KRAS -mutant AsPC-1 cells. b, SHANK3 mRNA levels. c, Representative images and quantification (mean ± s.d.) of the spheroid areas from n = 3 independent experiments. Unpaired Student’s t-test with Welch’s correction (at the endpoint). d, A schematic illustration of the chick embryo chorioallantoic membrane (CAM) xenograft assay.

    Techniques Used: Expressing, Transformation Assay, Mutagenesis, Xenograft Assay

    panc10 05  (ATCC)


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    ATCC panc10 05
    Panc10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    panc 10 05 crl 2547 cell lines  (ATCC)


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    ATCC panc 10 05 crl 2547 cell lines
    Panc 10 05 Crl 2547 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
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    panc10 05  (ATCC)


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    ATCC panc10 05
    (A) Long-term colony-formation assays of Aspc1, DLD-1, SUM159, Miapaca2, <t>Panc10.05,</t> Panc1, A549, H2122, HCC-1806, and HCT-116. Cells were treated with indicated doses of indisulam for 8–11 d. (B) Western blot analysis of RBM39 levels in Aspc1, DLD-1, SUM159, Miapaca2, Panc10.05, Panc1, A549, H2122, HCC-1806, and HCT-116 cells treated with 0.5 μM of indisulam for the indicated time periods. GAPDH was used as a loading control. (C) Dropout CRISPR screen was performed in A549 treated with 0.35 μM indisulam. Volcano plot of indisulam-treated samples compared with untreated. X axis shows log 2 fold change of normalized read counts and Y axis shows false discovery rate (FDR). Each dot represents an individual gene and SRPK1 is highlighted. (D) Western blot analysis of SRPK1 levels in A549 and SUM159 SRPK1 knock-out clones and control cells. Clones were generated from two independent sgRNAs. GAPDH was used as a loading control. (E) Long-term colony-formation assay of Α549 cells. A549 SRPK1 knock-out clones and control cells were treated with indicated doses of indisulam for 10 d. (F) Long-term colony-formation assay of SUM159 cells. SUM159 SRPK1 knock-out clones and control cells were treated with indicated doses of indisulam for 7 d. (G) Proliferation assay of A549 control and sgSRPK1 cells treated with 0.75 μM indisulam. One clone per sgRNA is shown. Mean of three technical replicates is shown and error bars indicate SD. (H) Proliferation assay of SUM159 control and sgSRPK1 cells treated with 1 μM indisulam. One clone per sgRNA is shown. Mean of three technical replicates is shown and error bars indicate SD. Source data are available for this figure.
    Panc10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Genetic and compound screens uncover factors modulating cancer cell response to indisulam"

    Article Title: Genetic and compound screens uncover factors modulating cancer cell response to indisulam

    Journal: Life Science Alliance

    doi: 10.26508/lsa.202101348

    (A) Long-term colony-formation assays of Aspc1, DLD-1, SUM159, Miapaca2, Panc10.05, Panc1, A549, H2122, HCC-1806, and HCT-116. Cells were treated with indicated doses of indisulam for 8–11 d. (B) Western blot analysis of RBM39 levels in Aspc1, DLD-1, SUM159, Miapaca2, Panc10.05, Panc1, A549, H2122, HCC-1806, and HCT-116 cells treated with 0.5 μM of indisulam for the indicated time periods. GAPDH was used as a loading control. (C) Dropout CRISPR screen was performed in A549 treated with 0.35 μM indisulam. Volcano plot of indisulam-treated samples compared with untreated. X axis shows log 2 fold change of normalized read counts and Y axis shows false discovery rate (FDR). Each dot represents an individual gene and SRPK1 is highlighted. (D) Western blot analysis of SRPK1 levels in A549 and SUM159 SRPK1 knock-out clones and control cells. Clones were generated from two independent sgRNAs. GAPDH was used as a loading control. (E) Long-term colony-formation assay of Α549 cells. A549 SRPK1 knock-out clones and control cells were treated with indicated doses of indisulam for 10 d. (F) Long-term colony-formation assay of SUM159 cells. SUM159 SRPK1 knock-out clones and control cells were treated with indicated doses of indisulam for 7 d. (G) Proliferation assay of A549 control and sgSRPK1 cells treated with 0.75 μM indisulam. One clone per sgRNA is shown. Mean of three technical replicates is shown and error bars indicate SD. (H) Proliferation assay of SUM159 control and sgSRPK1 cells treated with 1 μM indisulam. One clone per sgRNA is shown. Mean of three technical replicates is shown and error bars indicate SD. Source data are available for this figure.
    Figure Legend Snippet: (A) Long-term colony-formation assays of Aspc1, DLD-1, SUM159, Miapaca2, Panc10.05, Panc1, A549, H2122, HCC-1806, and HCT-116. Cells were treated with indicated doses of indisulam for 8–11 d. (B) Western blot analysis of RBM39 levels in Aspc1, DLD-1, SUM159, Miapaca2, Panc10.05, Panc1, A549, H2122, HCC-1806, and HCT-116 cells treated with 0.5 μM of indisulam for the indicated time periods. GAPDH was used as a loading control. (C) Dropout CRISPR screen was performed in A549 treated with 0.35 μM indisulam. Volcano plot of indisulam-treated samples compared with untreated. X axis shows log 2 fold change of normalized read counts and Y axis shows false discovery rate (FDR). Each dot represents an individual gene and SRPK1 is highlighted. (D) Western blot analysis of SRPK1 levels in A549 and SUM159 SRPK1 knock-out clones and control cells. Clones were generated from two independent sgRNAs. GAPDH was used as a loading control. (E) Long-term colony-formation assay of Α549 cells. A549 SRPK1 knock-out clones and control cells were treated with indicated doses of indisulam for 10 d. (F) Long-term colony-formation assay of SUM159 cells. SUM159 SRPK1 knock-out clones and control cells were treated with indicated doses of indisulam for 7 d. (G) Proliferation assay of A549 control and sgSRPK1 cells treated with 0.75 μM indisulam. One clone per sgRNA is shown. Mean of three technical replicates is shown and error bars indicate SD. (H) Proliferation assay of SUM159 control and sgSRPK1 cells treated with 1 μM indisulam. One clone per sgRNA is shown. Mean of three technical replicates is shown and error bars indicate SD. Source data are available for this figure.

    Techniques Used: Western Blot, CRISPR, Knock-Out, Clone Assay, Generated, Colony Assay, Proliferation Assay

    (A) Resistance screen was performed in A549 cells treated with 3 μM indisulam. Volcano plot of indisulam-treated samples compared with untreated. X axis shows log 2 fold change of normalized read counts and Y axis shows false discovery rate (FDR). Each dot represents an individual gene and hits are highlighted. (B) Proliferation assay of A549 control (sgCTRL) and sgCAND1 cells treated with 1 μM indisulam. Mean of three technical replicates is shown and error bars indicate SD. (C) Long-term colony-formation assay of A549. Wild-type, control, and two individual sgCAND1 cells were treated with indicated doses of indisulam for 10 d. (D) Western blot analysis of RBM39 and CAND1 in A549 cells. Wild-type, control and sgCAND1 cells were treated with 0.5 μM of indisulam for 8 d. GAPDH was used as loading control. (E) Long-term colony-formation assay of Panc10.05. Wild-type, control (sgCTRL), and two individual sgCAND1 cells were treated with indicated doses of indisulam for indicated number of d. (F) Western blot analysis of RBM39 and CAND1 in Panc10.05 cells. Wild-type, control, and sgCAND1 cells were treated with 0.5 μM of indisulam for 8 d. GAPDH was used as loading control. (G) CUL4-DCAF15 E3 ubiquitin ligase (CRL) complexes get activated by neddylation (N8) which allows ubiquitination of the substrate (RBM39). Neddylation is reversed by NEDD8-activating enzyme (NAE), which can be inhibited by a small molecular inhibitor MLN4924 leading to inactive CRL complex and reduced substrate degradation. (H) Western blot analysis of RBM39 and CUL4A in HCT-116 and A549 cells pretreated for 2 h with 1 μM MLN4924 or 5 μM MG-132 followed by a 6-h treatment with 0.5 μM indisulam. GAPDH was used as loading control. The upper CUL4A band (arrow) represents neddylated CUL4A, whereas the lower band represents the deneddylated CUL4A. (I) Western blot analysis of RBM39 and CUL4A in HCT-116 (62.5, 125 and 250 nM MLN4924) and A549 (125, 250, and 500 nM MLN4924) cells treated with 0.5 μM indisulam and increasing doses of MLN4924 for 24 h. The upper CUL4A band (arrow) represents neddylated CUL4A, whereas the lower band represents the deneddylated CUL4A. (J) Long-term colony-formation assays of HCT-116 (62.5 nM MLN4924), HCC-1806 (62.5 nM MLN4924), and A549 (125 nM MLN4924) treated with indicated doses of indisulam and a fixed concentration of MLN4924 for 8–13 d depending on the cell line. Source data are available for this figure.
    Figure Legend Snippet: (A) Resistance screen was performed in A549 cells treated with 3 μM indisulam. Volcano plot of indisulam-treated samples compared with untreated. X axis shows log 2 fold change of normalized read counts and Y axis shows false discovery rate (FDR). Each dot represents an individual gene and hits are highlighted. (B) Proliferation assay of A549 control (sgCTRL) and sgCAND1 cells treated with 1 μM indisulam. Mean of three technical replicates is shown and error bars indicate SD. (C) Long-term colony-formation assay of A549. Wild-type, control, and two individual sgCAND1 cells were treated with indicated doses of indisulam for 10 d. (D) Western blot analysis of RBM39 and CAND1 in A549 cells. Wild-type, control and sgCAND1 cells were treated with 0.5 μM of indisulam for 8 d. GAPDH was used as loading control. (E) Long-term colony-formation assay of Panc10.05. Wild-type, control (sgCTRL), and two individual sgCAND1 cells were treated with indicated doses of indisulam for indicated number of d. (F) Western blot analysis of RBM39 and CAND1 in Panc10.05 cells. Wild-type, control, and sgCAND1 cells were treated with 0.5 μM of indisulam for 8 d. GAPDH was used as loading control. (G) CUL4-DCAF15 E3 ubiquitin ligase (CRL) complexes get activated by neddylation (N8) which allows ubiquitination of the substrate (RBM39). Neddylation is reversed by NEDD8-activating enzyme (NAE), which can be inhibited by a small molecular inhibitor MLN4924 leading to inactive CRL complex and reduced substrate degradation. (H) Western blot analysis of RBM39 and CUL4A in HCT-116 and A549 cells pretreated for 2 h with 1 μM MLN4924 or 5 μM MG-132 followed by a 6-h treatment with 0.5 μM indisulam. GAPDH was used as loading control. The upper CUL4A band (arrow) represents neddylated CUL4A, whereas the lower band represents the deneddylated CUL4A. (I) Western blot analysis of RBM39 and CUL4A in HCT-116 (62.5, 125 and 250 nM MLN4924) and A549 (125, 250, and 500 nM MLN4924) cells treated with 0.5 μM indisulam and increasing doses of MLN4924 for 24 h. The upper CUL4A band (arrow) represents neddylated CUL4A, whereas the lower band represents the deneddylated CUL4A. (J) Long-term colony-formation assays of HCT-116 (62.5 nM MLN4924), HCC-1806 (62.5 nM MLN4924), and A549 (125 nM MLN4924) treated with indicated doses of indisulam and a fixed concentration of MLN4924 for 8–13 d depending on the cell line. Source data are available for this figure.

    Techniques Used: Proliferation Assay, Colony Assay, Western Blot, Concentration Assay

    (A) CAND1 gene editing efficiency in A549 sgCAND1-1 and sgCAND1-5 cells determined by TIDE analysis. (B) CAND1 gene editing efficiency in PANC10.05 sgCAND1-1 and sgCAND1-5 cells determined by TIDE analysis. (C) CAND1 gene editing efficiency in HCT-116 sgCAND1-1 and sgCAND1-5 cells determined by TIDE analysis. (D) Long-term colony-formation assay of HCT-116. Wild-type, control, and two individual sgCAND1 cells were treated with indicated doses of indisulam for indicated number of days. (E) Western blot analysis of RBM39 and CAND1 in HCT-116 cells. Wild-type, control, and sgCAND1 cells were treated with 0.125 μM of indisulam for 8 d. GAPDH was used as loading control. (F) Drug synergy analysis of indisulam and MLN4924 combination in HCT-116 and A549 cells. Mean of three biological replicates is shown and error bars indicate SD. (G) 3D representation of the synergy matrix of indisulam and MLN4924 in HCT-116 and A549 cells. Red areas represent high Bliss score and green areas represent low Bliss score. Mean of three biological replicates is shown.
    Figure Legend Snippet: (A) CAND1 gene editing efficiency in A549 sgCAND1-1 and sgCAND1-5 cells determined by TIDE analysis. (B) CAND1 gene editing efficiency in PANC10.05 sgCAND1-1 and sgCAND1-5 cells determined by TIDE analysis. (C) CAND1 gene editing efficiency in HCT-116 sgCAND1-1 and sgCAND1-5 cells determined by TIDE analysis. (D) Long-term colony-formation assay of HCT-116. Wild-type, control, and two individual sgCAND1 cells were treated with indicated doses of indisulam for indicated number of days. (E) Western blot analysis of RBM39 and CAND1 in HCT-116 cells. Wild-type, control, and sgCAND1 cells were treated with 0.125 μM of indisulam for 8 d. GAPDH was used as loading control. (F) Drug synergy analysis of indisulam and MLN4924 combination in HCT-116 and A549 cells. Mean of three biological replicates is shown and error bars indicate SD. (G) 3D representation of the synergy matrix of indisulam and MLN4924 in HCT-116 and A549 cells. Red areas represent high Bliss score and green areas represent low Bliss score. Mean of three biological replicates is shown.

    Techniques Used: Colony Assay, Western Blot

    (A) Long-term colony-formation assays of HCT-116(R), HCC-1806(R), A549(R), and Panc10.05(R) treated with indicated doses of indisulam for 8–10 d. (B) Quantification of cell viability of HCT-116(R), HCC-1806(R), A549(R), and Panc10.05(R) treated with a dilution series of indisulam. Mean of three technical replicates is shown and error bars indicate SD. (C) Western blot analysis of RBM39 in parental and resistant HCT-116, HCC-1806, A549, and Panc10.05. Tubulin was used as loading control. (D) Experimental design is described in panel (D). (D) Parental cells were treated for 24 h with 0.5 μM of indisulam. Resistant cells were cultured without indisulam for 1 wk (drug holiday, DH) and then treated for 24 h with 0.5 μM of indisulam or cultured continuously in the presence of 0.5 μM indisulam. (E) Quantification of splicing errors in RNA sequencing data from Panc10.05 cells treated for 18 h with 2 μM indisulam and Panc10.05R cells cultured on 2 μΜ indisulam. Resistant cells cultured without indisulam for 1 wk were considered untreated. Data were analyzed based on two technical replicates and bars represent the number of events compared with untreated samples. (F) Compound screen in resistant and parental Panc10.05 cells. Dose response curves of various compounds were generated. Comparison of area under the curve of parental versus resistant Panc10.05 is plotted for every compound. Compounds validated after a secondary screen are highlighted. (G) Cell viability of Panc10.05(R) cells treated with ABT-263 and A-1155463. Indisulam-resistant cells were cultured in the presence of 0.5 μM indisulam. Mean of three biological replicates is shown and error bars indicate SD. (H) Western blot analysis of BCL-xL in Panc10.05 parental and resistant cells. Parental cells were treated with 0.5 μM of indisulam for 24 h and resistant cells were cultured in the presence of 0.5 μΜ indisulam. Vinculin was used as a loading control. (I) Heat map of delta cytochrome c release compared with parental untreated cells (%) in Panc10.05(R) cells after BH3 profiling with A-1331852, BAD, HRK, and ABT-263. Before profiling, parental Panc10.05 cells were treated with 0.5 μM of indisulam for 24 h. Resistant Panc10.05 cells were cultured in the absence of indisulam for 2 wk and treated Panc10.05R cells were cultured in the presence of 0.5 μΜ indisulam. Mean of three technical replicates is shown. (J) Long-term colony-formation assay of Panc10.05 cells treated with 2 μM ABT-263, 2 μM A-1155463, 4 μM indisulam, and the combinations for the indicated duration. Representative image of three independent biological replicates is shown. (K) Quantification of long-term colony-formation assays of Panc10.05. Mean of three biological replicates is shown and error bars indicate SD. Source data are available for this figure.
    Figure Legend Snippet: (A) Long-term colony-formation assays of HCT-116(R), HCC-1806(R), A549(R), and Panc10.05(R) treated with indicated doses of indisulam for 8–10 d. (B) Quantification of cell viability of HCT-116(R), HCC-1806(R), A549(R), and Panc10.05(R) treated with a dilution series of indisulam. Mean of three technical replicates is shown and error bars indicate SD. (C) Western blot analysis of RBM39 in parental and resistant HCT-116, HCC-1806, A549, and Panc10.05. Tubulin was used as loading control. (D) Experimental design is described in panel (D). (D) Parental cells were treated for 24 h with 0.5 μM of indisulam. Resistant cells were cultured without indisulam for 1 wk (drug holiday, DH) and then treated for 24 h with 0.5 μM of indisulam or cultured continuously in the presence of 0.5 μM indisulam. (E) Quantification of splicing errors in RNA sequencing data from Panc10.05 cells treated for 18 h with 2 μM indisulam and Panc10.05R cells cultured on 2 μΜ indisulam. Resistant cells cultured without indisulam for 1 wk were considered untreated. Data were analyzed based on two technical replicates and bars represent the number of events compared with untreated samples. (F) Compound screen in resistant and parental Panc10.05 cells. Dose response curves of various compounds were generated. Comparison of area under the curve of parental versus resistant Panc10.05 is plotted for every compound. Compounds validated after a secondary screen are highlighted. (G) Cell viability of Panc10.05(R) cells treated with ABT-263 and A-1155463. Indisulam-resistant cells were cultured in the presence of 0.5 μM indisulam. Mean of three biological replicates is shown and error bars indicate SD. (H) Western blot analysis of BCL-xL in Panc10.05 parental and resistant cells. Parental cells were treated with 0.5 μM of indisulam for 24 h and resistant cells were cultured in the presence of 0.5 μΜ indisulam. Vinculin was used as a loading control. (I) Heat map of delta cytochrome c release compared with parental untreated cells (%) in Panc10.05(R) cells after BH3 profiling with A-1331852, BAD, HRK, and ABT-263. Before profiling, parental Panc10.05 cells were treated with 0.5 μM of indisulam for 24 h. Resistant Panc10.05 cells were cultured in the absence of indisulam for 2 wk and treated Panc10.05R cells were cultured in the presence of 0.5 μΜ indisulam. Mean of three technical replicates is shown. (J) Long-term colony-formation assay of Panc10.05 cells treated with 2 μM ABT-263, 2 μM A-1155463, 4 μM indisulam, and the combinations for the indicated duration. Representative image of three independent biological replicates is shown. (K) Quantification of long-term colony-formation assays of Panc10.05. Mean of three biological replicates is shown and error bars indicate SD. Source data are available for this figure.

    Techniques Used: Western Blot, Cell Culture, RNA Sequencing Assay, Generated, Colony Assay

    (A) Western blot analysis of CAND1 in parental and resistant HCT-116, HCC-1806, A549, and Panc10.05. GAPDH was used as loading control. Experimental design is described in . (B) Cell viability of A549(R) and HCC-1806(R) cells treated with ABT-263 and A-1155463. Indisulam-resistant cells were cultured in the presence of 0.5 μM indisulam. Mean of three biological replicates is shown and error bars indicate SD. (C) Long-term colony-formation assays of Panc1, Miapaca2, and Aspc1. Both Miapaca2 and Aspc1 were treated with 2 μM ABT-263, 2 μM A-1155463, 4 μΜ indisulam, and the combination for the indicated duration. Panc1 was treated with 1 μM ABT-263, 3 μM A-1155463, 1 μM indisulam, and the combination. (D) Quantification of long-term colony-formation assays of Panc1, Miapaca2, and Aspc1 cells. Mean of three biological replicates is shown and error bars indicate SD. (E) Western blot analysis of BCL-2, Bcl-xL, and RBM39 in Panc10.05, Miapaca2, Aspc1 and Panc1 parental and resistant cells. Parental cells were treated with 0.5 μM of indisulam for 24 h and resistant cells were cultured in the presence of 0.5 μΜ indisulam. Vinculin was used as a loading control.
    Figure Legend Snippet: (A) Western blot analysis of CAND1 in parental and resistant HCT-116, HCC-1806, A549, and Panc10.05. GAPDH was used as loading control. Experimental design is described in . (B) Cell viability of A549(R) and HCC-1806(R) cells treated with ABT-263 and A-1155463. Indisulam-resistant cells were cultured in the presence of 0.5 μM indisulam. Mean of three biological replicates is shown and error bars indicate SD. (C) Long-term colony-formation assays of Panc1, Miapaca2, and Aspc1. Both Miapaca2 and Aspc1 were treated with 2 μM ABT-263, 2 μM A-1155463, 4 μΜ indisulam, and the combination for the indicated duration. Panc1 was treated with 1 μM ABT-263, 3 μM A-1155463, 1 μM indisulam, and the combination. (D) Quantification of long-term colony-formation assays of Panc1, Miapaca2, and Aspc1 cells. Mean of three biological replicates is shown and error bars indicate SD. (E) Western blot analysis of BCL-2, Bcl-xL, and RBM39 in Panc10.05, Miapaca2, Aspc1 and Panc1 parental and resistant cells. Parental cells were treated with 0.5 μM of indisulam for 24 h and resistant cells were cultured in the presence of 0.5 μΜ indisulam. Vinculin was used as a loading control.

    Techniques Used: Western Blot, Cell Culture

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    ATCC panc 10 05
    Panc 10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC crl 2547
    H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: <t>CRL-2547,</t> CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.
    Crl 2547, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC panc10 05 cells
    H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: <t>CRL-2547,</t> CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.
    Panc10 05 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC panc10 05
    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and <t>Panc10.05</t> (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Panc10 05, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    crl  (ATCC)
    99
    ATCC crl
    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and <t>Panc10.05</t> (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Crl, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    ATCC panc 10 05 crl 2547 cell lines
    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and <t>Panc10.05</t> (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " width="250" height="auto" />
    Panc 10 05 Crl 2547 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
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    H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: CRL-2547, CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.

    Journal: Journal of Oncology

    Article Title: Use of H19 Gene Regulatory Sequences in DNA-Based Therapy for Pancreatic Cancer

    doi: 10.1155/2010/178174

    Figure Lengend Snippet: H19 RNA level in human and hamster pancreatic carcinoma cell lines. (a) Lane 1: 100 bp marker, Lane 2: CRL-1469 cells, Lane 3: PC.1-0 hamster cells. (b) Lane 1: 100 bp marker, Lanes 2–5: CRL-2547, CRL-1687, CRL-2119, and CRL-1997 human pancreatic carcinoma cells, respectively. (c) Lane 1: 100 bp marker; Lane 2: mouse control; Lane 3: PC.1-0 cells cultured under normoxia conditions; Lane 4: PC.1-0 cells cultured under hypoxia condition for 4 hours; Lane 5: tumors generated by PC.1-0 cells injection into nude mice back; Lane 6: negative control, no cDNA is present in the reaction mixture. The upper and the middle panels show the 228 bp and the 454 bp PCR products, respectively, obtained using two different primers (H19-mouse 228 and H19-mouse 454 as described in Supplementary data, Table A). The lower panel indicates the 400 bp β -actin internal control.

    Article Snippet: Human pancreatic adenocarcinoma cell lines CRL-1687, CRL-2119, CRL-1997, and CRL-2547 and ductal adenocarcinoma cell line CRL-1469 were obtained from the American Type Culture Collection (ATCC; Rockville, MD, USA) and cultured in 90% DMEM-F12 medium and 10% Fetal Bovine Serum (FBS).

    Techniques: Marker, Cell Culture, Generated, Injection, Negative Control

    Heterotopic model for pancreatic cancer. (a) Average tumor volume of Luc-H19 group ( n = 8) and DTA-H19 group ( n = 7) during the experiment using CRL-1469 cells. Treatments were administrated on days 0, 3, and 6 by direct intratumoral injection after subcutaneous implantation of human pancreatic carcinoma cells in the back of nude mice. Three days after the last treatment, the animals were sacrificed. (b) Average of ex vivo tumor volume at the end of the experiment, tumors generated using CRL-1469 cells. (c) Tumor Growth Progression of Luc-H19 ( n = 5) and DTA-H19 ( n = 5) groups, in experiment using CRL-2547 cell line.

    Journal: Journal of Oncology

    Article Title: Use of H19 Gene Regulatory Sequences in DNA-Based Therapy for Pancreatic Cancer

    doi: 10.1155/2010/178174

    Figure Lengend Snippet: Heterotopic model for pancreatic cancer. (a) Average tumor volume of Luc-H19 group ( n = 8) and DTA-H19 group ( n = 7) during the experiment using CRL-1469 cells. Treatments were administrated on days 0, 3, and 6 by direct intratumoral injection after subcutaneous implantation of human pancreatic carcinoma cells in the back of nude mice. Three days after the last treatment, the animals were sacrificed. (b) Average of ex vivo tumor volume at the end of the experiment, tumors generated using CRL-1469 cells. (c) Tumor Growth Progression of Luc-H19 ( n = 5) and DTA-H19 ( n = 5) groups, in experiment using CRL-2547 cell line.

    Article Snippet: Human pancreatic adenocarcinoma cell lines CRL-1687, CRL-2119, CRL-1997, and CRL-2547 and ductal adenocarcinoma cell line CRL-1469 were obtained from the American Type Culture Collection (ATCC; Rockville, MD, USA) and cultured in 90% DMEM-F12 medium and 10% Fetal Bovine Serum (FBS).

    Techniques: Injection, Ex Vivo, Generated

    Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also <xref ref-type=Figure S1 . " width="100%" height="100%">

    Journal: Cell Reports Medicine

    Article Title: Extensive preclinical validation of combined RMC-4550 and LY3214996 supports clinical investigation for KRAS mutant pancreatic cancer

    doi: 10.1016/j.xcrm.2022.100815

    Figure Lengend Snippet: Evaluation of the combined effects of RMC-4550 (SHP2i) and LY3214996 (ERKi) administration in murine and human KRAS -mutant pancreatic cancer cell lines (A) Western blot analysis with murine cancer cell line KCP_K2101 derived from KCP mouse model (KRAS G12D ) of spontaneous tumor formation and in human cancer cell lines: MiaPaCa-2 (KRAS G12C ) and Panc10.05 (KRAS G12D ). Cells were treated as depicted and collected for lysis at the indicated time points. Protein extracts were probed with specific antibodies against total RSK-1, phosphorylated RSK-1 (pRSK-1), and alpha-tubulin (as loading control). Numerical values indicate the pRSK-1/RSK-1 ratio quantified by densitometry. The blots are representative of at least three independent experiments. RSK-1, ribosomal S6 kinase 1. (B) Synergistic effects of SHP2i and ERKi administration were evaluated by colony-formation assay in the KRAS -mutant cell lines used in (A). SHP2i and ERKi were combined at the indicated concentrations. Representative crystal violet staining of cells is shown (top panel). Box matrices below the plate scans depict quantification of growth inhibition in relation to control wells (middle panel). Bottom panel: calculation of the combination index (CI) scores from the growth inhibition values (shown above) via CompuSyn software demonstrating strong synergism between SHP2i and ERKi across a wide range of combinatorial concentrations. CI <0.75 (shades of green) indicates synergism, CI = 0.75–1.25 (shades of blue) indicates additive effects, and CI >1.25 (shades of red) indicates antagonism. Experiments were repeated independently at least three times each, with similar results. (C) Apoptosis was analyzed in cell lines treated with either DMSO, SHP2i alone, ERKi alone, or a combination of SHP2i and ERKi at the indicated concentration in real time (top panel). GFP signal coupled to cleaved caspase 3 was quantified as readout. Bar plots for selected time points (48 h for KCP_K2101 and 76 h for MiaPaCa-2 and Panc10.05) show the fraction of GFP-positive cells (AU) (top panel) and the fold change GFP signal (bottom panel). AU, arbitrary units; GFP, green fluorescent protein. Experiments were repeated independently at least three times each. Results represent mean ± SD. ∗p < 0.05, ∗∗∗∗p < 0.0001, as determined by ordinary one-way ANOVA test. See also Figure S1 .

    Article Snippet: Panc10.05 , ATCC , CRL-2547; RRID: CVCL_1639.

    Techniques: Mutagenesis, Western Blot, Derivative Assay, Lysis, Colony Assay, Staining, Inhibition, Software, Concentration Assay

    Journal: Cell Reports Medicine

    Article Title: Extensive preclinical validation of combined RMC-4550 and LY3214996 supports clinical investigation for KRAS mutant pancreatic cancer

    doi: 10.1016/j.xcrm.2022.100815

    Figure Lengend Snippet:

    Article Snippet: Panc10.05 , ATCC , CRL-2547; RRID: CVCL_1639.

    Techniques: Derivative Assay, Recombinant, Western Blot, Mouse Assay, Software