anti inflammatory regulators  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti inflammatory regulators
    Anti Inflammatory Regulators, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti inflammatory regulators  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti inflammatory regulators
    Anti Inflammatory Regulators, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti enolase 1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti enolase 1
    Anti Enolase 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti eno1 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti eno1 antibody
    A: Activity of immuno-captured <t>α-enolase</t> <t>(ENO1)</t> from HEK293T cells after stimulation with insulin and AKT-inhibition with CCT128930. Data represent means ± SD of n = 7 experiments. B: Detection of immuno-captured α-enolase after α-enolase activity assay. After detection of α-enolase blots were incubated with anti-pan AKT antibody. Note that AKT was also detected after isolation of α-enolase by the α-enolase antibody.
    Anti Eno1 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 1 article reviews
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    anti eno1 antibody - by Bioz Stars, 2023-01
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    1) Product Images from "Systematic Analysis Reveals Elongation Factor 2 and α-Enolase as Novel Interaction Partners of AKT2"

    Article Title: Systematic Analysis Reveals Elongation Factor 2 and α-Enolase as Novel Interaction Partners of AKT2

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0066045

    A: Activity of immuno-captured α-enolase (ENO1) from HEK293T cells after stimulation with insulin and AKT-inhibition with CCT128930. Data represent means ± SD of n = 7 experiments. B: Detection of immuno-captured α-enolase after α-enolase activity assay. After detection of α-enolase blots were incubated with anti-pan AKT antibody. Note that AKT was also detected after isolation of α-enolase by the α-enolase antibody.
    Figure Legend Snippet: A: Activity of immuno-captured α-enolase (ENO1) from HEK293T cells after stimulation with insulin and AKT-inhibition with CCT128930. Data represent means ± SD of n = 7 experiments. B: Detection of immuno-captured α-enolase after α-enolase activity assay. After detection of α-enolase blots were incubated with anti-pan AKT antibody. Note that AKT was also detected after isolation of α-enolase by the α-enolase antibody.

    Techniques Used: Activity Assay, Inhibition, Incubation, Isolation

    eno1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc eno1
    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) <t>Enolase</t> <t>1</t> <t>(Eno1),</t> Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
    Eno1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs"

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    Journal: Theranostics

    doi: 10.7150/thno.70549

    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
    Figure Legend Snippet: Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Techniques Used: Mass Spectrometry, Derivative Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Recombinant

    Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.
    Figure Legend Snippet: Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Techniques Used: Over Expression, Recombinant, Immunoprecipitation, Western Blot, Mutagenesis, Pull Down Assay, Negative Control, Plasmid Preparation, Transfection

    Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.
    Figure Legend Snippet: Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Techniques Used: Recombinant, Over Expression, Derivative Assay

    antibodies against eno1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies against eno1
    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) <t>Enolase</t> <t>1</t> <t>(Eno1),</t> Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
    Antibodies Against Eno1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against eno1/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against eno1 - by Bioz Stars, 2023-01
    95/100 stars

    Images

    1) Product Images from "Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs"

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    Journal: Theranostics

    doi: 10.7150/thno.70549

    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
    Figure Legend Snippet: Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Techniques Used: Mass Spectrometry, Derivative Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Recombinant

    Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.
    Figure Legend Snippet: Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Techniques Used: Over Expression, Recombinant, Immunoprecipitation, Western Blot, Mutagenesis, Pull Down Assay, Negative Control, Plasmid Preparation, Transfection

    Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.
    Figure Legend Snippet: Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Techniques Used: Recombinant, Over Expression, Derivative Assay

    anti eno1 antibodies  (Cell Signaling Technology Inc)


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    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Structured Review

    Cell Signaling Technology Inc anti eno1 antibodies
    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) <t>Enolase</t> <t>1</t> <t>(Eno1),</t> Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
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    Images

    1) Product Images from "Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs"

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    Journal: Theranostics

    doi: 10.7150/thno.70549

    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
    Figure Legend Snippet: Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Techniques Used: Mass Spectrometry, Derivative Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Recombinant

    Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.
    Figure Legend Snippet: Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Techniques Used: Over Expression, Recombinant, Immunoprecipitation, Western Blot, Mutagenesis, Pull Down Assay, Negative Control, Plasmid Preparation, Transfection

    Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.
    Figure Legend Snippet: Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Techniques Used: Recombinant, Over Expression, Derivative Assay

    eno1  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc eno1
    Mass spectrometry-based prediction of tumor suppressors and the effect of <t>enolase</t> <t>1</t> and ubiquitin C. EO = EO771 mammary tumor cells, CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, BML = BML284, <t>Eno1</t> = Enolase 1, and Ubc = ubiquitin C. The single and double asterisks indicate p < 0.05 and p < 0.01, respectively. (A) List of 25 top tumor suppressor candidates identified by mass spectrometry-based proteomics analysis. (B) Reduction in MTT-based proliferation of EO771 mammary tumor cells by 9 recombinant proteins (5 μg/mL) in 48 h. (C) Levels of enolase 1 and ubiquitin C in β-catenin-overexpressing and BML284-treated EO771 CMs by ELISA. (D) Inhibition in the scratch-based migration of EO771 mammary tumor cells by enolase 1 and ubiquitin C in 24 h. (E) Expression of β-catenin and enolase 1 in EO771 cells that were treated with AP-Ⅲ-a4, an inhibitor of enolase 1. (F&G) Repressive effects of AP-Ⅲ-a4 on the proliferation (in 48 h) and migration of EO771 cells (in 24 h) by β-catenin overexpressing iTS CM.
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    1) Product Images from "Generation of the tumor-suppressive secretome from tumor cells"

    Article Title: Generation of the tumor-suppressive secretome from tumor cells

    Journal: Theranostics

    doi: 10.7150/thno.61006

    Mass spectrometry-based prediction of tumor suppressors and the effect of enolase 1 and ubiquitin C. EO = EO771 mammary tumor cells, CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, BML = BML284, Eno1 = Enolase 1, and Ubc = ubiquitin C. The single and double asterisks indicate p < 0.05 and p < 0.01, respectively. (A) List of 25 top tumor suppressor candidates identified by mass spectrometry-based proteomics analysis. (B) Reduction in MTT-based proliferation of EO771 mammary tumor cells by 9 recombinant proteins (5 μg/mL) in 48 h. (C) Levels of enolase 1 and ubiquitin C in β-catenin-overexpressing and BML284-treated EO771 CMs by ELISA. (D) Inhibition in the scratch-based migration of EO771 mammary tumor cells by enolase 1 and ubiquitin C in 24 h. (E) Expression of β-catenin and enolase 1 in EO771 cells that were treated with AP-Ⅲ-a4, an inhibitor of enolase 1. (F&G) Repressive effects of AP-Ⅲ-a4 on the proliferation (in 48 h) and migration of EO771 cells (in 24 h) by β-catenin overexpressing iTS CM.
    Figure Legend Snippet: Mass spectrometry-based prediction of tumor suppressors and the effect of enolase 1 and ubiquitin C. EO = EO771 mammary tumor cells, CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, BML = BML284, Eno1 = Enolase 1, and Ubc = ubiquitin C. The single and double asterisks indicate p < 0.05 and p < 0.01, respectively. (A) List of 25 top tumor suppressor candidates identified by mass spectrometry-based proteomics analysis. (B) Reduction in MTT-based proliferation of EO771 mammary tumor cells by 9 recombinant proteins (5 μg/mL) in 48 h. (C) Levels of enolase 1 and ubiquitin C in β-catenin-overexpressing and BML284-treated EO771 CMs by ELISA. (D) Inhibition in the scratch-based migration of EO771 mammary tumor cells by enolase 1 and ubiquitin C in 24 h. (E) Expression of β-catenin and enolase 1 in EO771 cells that were treated with AP-Ⅲ-a4, an inhibitor of enolase 1. (F&G) Repressive effects of AP-Ⅲ-a4 on the proliferation (in 48 h) and migration of EO771 cells (in 24 h) by β-catenin overexpressing iTS CM.

    Techniques Used: Mass Spectrometry, Recombinant, Enzyme-linked Immunosorbent Assay, Inhibition, Migration, Expressing

    Effect of silencing enolase 1 and ubiquitin C. CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, siEno1 = Enolase 1 siRNA, siUbc = ubiquitin C siRNA, EO = EO771 mammary tumor cells, TR = TRAMP prostate cancer cells, and PA = PANC-1 pancreas cancer cells. The double asterisk indicates p < 0.01. (A) siRNA-mediated knockdown of enolase 1, and ubiquitin C in EO771 breast cancer cells. (B&C) Promotion of MTT-based proliferation, and scratch-based migration of EO771 breast cancer cells by enolase 1 and ubiquitin C siRNA-treated CMs in 2 days. (D-I) Effects of enolase 1 and ubiquitin C siRNAs. Silencing these two proteins significantly prevented the reduction in EdU-based proliferation and Transwell invasion of EO771, TRAMP, and PANC-1 cells by their own β-catenin-overexpressing iTS CMs in 2 days.
    Figure Legend Snippet: Effect of silencing enolase 1 and ubiquitin C. CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, siEno1 = Enolase 1 siRNA, siUbc = ubiquitin C siRNA, EO = EO771 mammary tumor cells, TR = TRAMP prostate cancer cells, and PA = PANC-1 pancreas cancer cells. The double asterisk indicates p < 0.01. (A) siRNA-mediated knockdown of enolase 1, and ubiquitin C in EO771 breast cancer cells. (B&C) Promotion of MTT-based proliferation, and scratch-based migration of EO771 breast cancer cells by enolase 1 and ubiquitin C siRNA-treated CMs in 2 days. (D-I) Effects of enolase 1 and ubiquitin C siRNAs. Silencing these two proteins significantly prevented the reduction in EdU-based proliferation and Transwell invasion of EO771, TRAMP, and PANC-1 cells by their own β-catenin-overexpressing iTS CMs in 2 days.

    Techniques Used: Migration

    Tumor selectivity and the involvement of CD44. A5 = MLO-A5 osteocytes, β-cat = β-catenin plasmids, BML = BML284, Eno1 = Enolase 1, Ubc = ubiquitin C. The signal and double asterisk indicates p < 0.01 and p < 0.05, respectively. (A) Comparison of MTT-based viability of four non-tumor cells (KTB34, KTB6, MC3T3, MSC) and four tumor cells (EO771, TRAMP, 4T1.2, PANC-1) in response to β-catenin-iTS CM and BML-iTS CM in 2 days. (B) Tumor selectivity of EO771 CM, 4T1.2 CM, TRAMP CM, and PANC-1 CM. MTT-based tumor selectivity is defined as the ratio of (reduction in tumor cells) to (reduction in non-tumor cells). The selectivity value above 1 indicates that MTT-based inhibition is more selective to tumor cells than non-tumor cells. Of note, N.D. = not defined since the viability of non-tumor cells is stimulated. (C&D) Tumor selectivity of Enolase 1 and ubiquitin C. (E) CD44 was co-immunoprecipitated with Eno1. The protein extracts of EO771 cells were incubated with anti-Eno1 antibody using the protein A/G beads. Immunoprecipitates and total cell lysates were analyzed by Western blotting with anti-CD44 and anti-Eno1 antibodies as indicated. (F&G) siRNA knockdown of CD44 suppressed Eno1-mediated inhibition of the proliferation of EO771 cells. (H) siRNA knockdown of CD44 suppressed Eno1-mediated downregulation of MMP9, Runx2, and Snail in EO771 cells.
    Figure Legend Snippet: Tumor selectivity and the involvement of CD44. A5 = MLO-A5 osteocytes, β-cat = β-catenin plasmids, BML = BML284, Eno1 = Enolase 1, Ubc = ubiquitin C. The signal and double asterisk indicates p < 0.01 and p < 0.05, respectively. (A) Comparison of MTT-based viability of four non-tumor cells (KTB34, KTB6, MC3T3, MSC) and four tumor cells (EO771, TRAMP, 4T1.2, PANC-1) in response to β-catenin-iTS CM and BML-iTS CM in 2 days. (B) Tumor selectivity of EO771 CM, 4T1.2 CM, TRAMP CM, and PANC-1 CM. MTT-based tumor selectivity is defined as the ratio of (reduction in tumor cells) to (reduction in non-tumor cells). The selectivity value above 1 indicates that MTT-based inhibition is more selective to tumor cells than non-tumor cells. Of note, N.D. = not defined since the viability of non-tumor cells is stimulated. (C&D) Tumor selectivity of Enolase 1 and ubiquitin C. (E) CD44 was co-immunoprecipitated with Eno1. The protein extracts of EO771 cells were incubated with anti-Eno1 antibody using the protein A/G beads. Immunoprecipitates and total cell lysates were analyzed by Western blotting with anti-CD44 and anti-Eno1 antibodies as indicated. (F&G) siRNA knockdown of CD44 suppressed Eno1-mediated inhibition of the proliferation of EO771 cells. (H) siRNA knockdown of CD44 suppressed Eno1-mediated downregulation of MMP9, Runx2, and Snail in EO771 cells.

    Techniques Used: Inhibition, Immunoprecipitation, Incubation, Western Blot

    Effects of enolase 1, ubiquitin C, and iTS CM on the expression of tumor-promoting and tumor-suppressing genes. CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, siEno1 = Enolase 1 siRNA, siUbc = ubiquitin C siRNA, EO = EO771 mammary tumor cells. (A&B) Expression of MMP9, Runx2, Snail, p53, and TRAIL in response to enolase 1 and ubiquitin C in EO771 breast cancer cells. (C&D) Expression of MMP9, Runx2, Snail, p53, and TRAIL in response to β-catenin-overexpressing iTS CM impaired by siRNAs specific to enolase 1 and ubiquitin C. (E) Expression of PDL1 in EO771 mammary tumor cells in response to β-catenin-overexpressing iTS CM, enolase 1, and ubiquitin C. (F&G) Expression of MMP9, Runx2, Snail, p53, TRAIL, and caspase 3 in EO771 mammary tumor cells in response to β-catenin-overexpressing pre-treatment tumor cell-derived CM. (H) Low survival for cancer patients with a high transcript level of MMP9, Runx2, or Snail. (I) Proposed regulatory mechanism to inhibit tumor progression by iTS-CM. According to the mechanism, β-catenin-overexpressing iTS cells secrete ubiquitin C (Ubc), enolase 1 (Eno1), p53, and Trail. They suppress the progression of tumor cells by downregulating MMP9, Runx2, Snail, and PDL1, while upregulating cleaved-caspase 3. It should be noted that Eno1 interacts with CD44 and inhibits MMP9, Runx2, and Snail.
    Figure Legend Snippet: Effects of enolase 1, ubiquitin C, and iTS CM on the expression of tumor-promoting and tumor-suppressing genes. CM = conditioned medium, CN = control (no CM treatment), β-cat = β-catenin plasmids, siEno1 = Enolase 1 siRNA, siUbc = ubiquitin C siRNA, EO = EO771 mammary tumor cells. (A&B) Expression of MMP9, Runx2, Snail, p53, and TRAIL in response to enolase 1 and ubiquitin C in EO771 breast cancer cells. (C&D) Expression of MMP9, Runx2, Snail, p53, and TRAIL in response to β-catenin-overexpressing iTS CM impaired by siRNAs specific to enolase 1 and ubiquitin C. (E) Expression of PDL1 in EO771 mammary tumor cells in response to β-catenin-overexpressing iTS CM, enolase 1, and ubiquitin C. (F&G) Expression of MMP9, Runx2, Snail, p53, TRAIL, and caspase 3 in EO771 mammary tumor cells in response to β-catenin-overexpressing pre-treatment tumor cell-derived CM. (H) Low survival for cancer patients with a high transcript level of MMP9, Runx2, or Snail. (I) Proposed regulatory mechanism to inhibit tumor progression by iTS-CM. According to the mechanism, β-catenin-overexpressing iTS cells secrete ubiquitin C (Ubc), enolase 1 (Eno1), p53, and Trail. They suppress the progression of tumor cells by downregulating MMP9, Runx2, Snail, and PDL1, while upregulating cleaved-caspase 3. It should be noted that Eno1 interacts with CD44 and inhibits MMP9, Runx2, and Snail.

    Techniques Used: Expressing, Derivative Assay

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    Cell Signaling Technology Inc eno1
    Liver lysosomes of fed Snell mice show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and Snell (S) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, <t>ENO1,</t> and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. (G) Representative western blots for binding and uptake assays for CMA substrate GAPDH, quantified in (H). (I) Representative western blots for binding and uptake assays for CMA substrate MAPT, quantified in (J). For (B-F), n = 9 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. For (H & J), n = 6 of each treatment group, the results of Student’s t-test are shown on the graphs. Error bars are S.E.M
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    1) Product Images from "Long-lived mice with reduced growth hormone signaling have a constitutive upregulation of hepatic chaperone-mediated autophagy"

    Article Title: Long-lived mice with reduced growth hormone signaling have a constitutive upregulation of hepatic chaperone-mediated autophagy

    Journal: Autophagy

    doi: 10.1080/15548627.2020.1725378

    Liver lysosomes of fed Snell mice show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and Snell (S) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, ENO1, and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. (G) Representative western blots for binding and uptake assays for CMA substrate GAPDH, quantified in (H). (I) Representative western blots for binding and uptake assays for CMA substrate MAPT, quantified in (J). For (B-F), n = 9 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. For (H & J), n = 6 of each treatment group, the results of Student’s t-test are shown on the graphs. Error bars are S.E.M
    Figure Legend Snippet: Liver lysosomes of fed Snell mice show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and Snell (S) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, ENO1, and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. (G) Representative western blots for binding and uptake assays for CMA substrate GAPDH, quantified in (H). (I) Representative western blots for binding and uptake assays for CMA substrate MAPT, quantified in (J). For (B-F), n = 9 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. For (H & J), n = 6 of each treatment group, the results of Student’s t-test are shown on the graphs. Error bars are S.E.M

    Techniques Used: Western Blot, Binding Assay

    Liver lysosomes of fed ghr KO mice show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and ghr KO (KO) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, ENO1, and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. (G) Representative western blots for binding and uptake assays for CMA substrate MAPT, quantified in (H). For (B-F), n = 6 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. For (H), n = 6 of each treatment group; the results of Student’s t-test are shown on the graphs. Error bars are S.E.M
    Figure Legend Snippet: Liver lysosomes of fed ghr KO mice show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and ghr KO (KO) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, ENO1, and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. (G) Representative western blots for binding and uptake assays for CMA substrate MAPT, quantified in (H). For (B-F), n = 6 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. For (H), n = 6 of each treatment group; the results of Student’s t-test are shown on the graphs. Error bars are S.E.M

    Techniques Used: Western Blot, Binding Assay

    Liver lysosomes of fed Li-ghr KO mice do not show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and Li-ghr KO (KO) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, ENO1, and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. For (B-F), n = 5 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. Error bars are S.E.M
    Figure Legend Snippet: Liver lysosomes of fed Li-ghr KO mice do not show more uptake of CMA substrates than lysosomes from littermate controls. (A) Representative western blots of liver lysosomes from control (C) and Li-ghr KO (KO) mice 2 h after treatments with leupeptin (100 mg/kg body weight) or PBS vehicle control. (B-D) Quantifications of the abundance of CMA substrates GAPDH, ENO1, and ACADL in lysosomes shown in (A). (E) Quantification of PPID, endosomal microautophagy substrate. (F) Quantification of HSPA8, CMA chaperone. For (B-F), n = 5 of each treatment group, 2-way ANOVA results are reported below each bar graph. Comparisons plotted on the bar graphs are results of Student’s t-test. Error bars are S.E.M

    Techniques Used: Western Blot

    anti enolase 1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti enolase 1
    Anti Enolase 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc eno1
    Tumor-suppressing proteins in CW008-treated MSC CM. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CM = conditioned medium, CW = CW008 (PKA activator), Calr = Calreticulin, <t>Eno1</t> = Enolase 1, Hsp90ab1 or Hsp = heat shock protein 90ab1, MSN = Moesin, Ubc = ubiquitin C, MMP2 and MMP9 = matrix metalloproteinases 2 and 9, Col I = type I collagen. (A) Western blot-based expression levels of Calr, Eno1, Hsp90ab1, MSN, Ubc, MMP2, MMP9, and Col I in CW008-treated MSC CM. (B-F) ELISA-based levels of 5 tumor-suppressing proteins (Calr, Eno1, Hsp90ab1, MSN, and Ubc) in CW008-treated MSC CM. (G) Dose responses of TT2 OS cells in response to CW008-treated MSC CM with IC 50 at 390 μg/mL. (H) Dose responses and IC 50 of TT2 OS cells in response to 5 tumor-suppressing proteins (Calr, Eno1, Hsp90ab1, MSN, and Ubc).
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    1) Product Images from "Osteosarcoma-enriched transcripts paradoxically generate osteosarcoma-suppressing extracellular proteins"

    Article Title: Osteosarcoma-enriched transcripts paradoxically generate osteosarcoma-suppressing extracellular proteins

    Journal: bioRxiv

    doi: 10.1101/2022.10.18.512687

    Tumor-suppressing proteins in CW008-treated MSC CM. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CM = conditioned medium, CW = CW008 (PKA activator), Calr = Calreticulin, Eno1 = Enolase 1, Hsp90ab1 or Hsp = heat shock protein 90ab1, MSN = Moesin, Ubc = ubiquitin C, MMP2 and MMP9 = matrix metalloproteinases 2 and 9, Col I = type I collagen. (A) Western blot-based expression levels of Calr, Eno1, Hsp90ab1, MSN, Ubc, MMP2, MMP9, and Col I in CW008-treated MSC CM. (B-F) ELISA-based levels of 5 tumor-suppressing proteins (Calr, Eno1, Hsp90ab1, MSN, and Ubc) in CW008-treated MSC CM. (G) Dose responses of TT2 OS cells in response to CW008-treated MSC CM with IC 50 at 390 μg/mL. (H) Dose responses and IC 50 of TT2 OS cells in response to 5 tumor-suppressing proteins (Calr, Eno1, Hsp90ab1, MSN, and Ubc).
    Figure Legend Snippet: Tumor-suppressing proteins in CW008-treated MSC CM. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CM = conditioned medium, CW = CW008 (PKA activator), Calr = Calreticulin, Eno1 = Enolase 1, Hsp90ab1 or Hsp = heat shock protein 90ab1, MSN = Moesin, Ubc = ubiquitin C, MMP2 and MMP9 = matrix metalloproteinases 2 and 9, Col I = type I collagen. (A) Western blot-based expression levels of Calr, Eno1, Hsp90ab1, MSN, Ubc, MMP2, MMP9, and Col I in CW008-treated MSC CM. (B-F) ELISA-based levels of 5 tumor-suppressing proteins (Calr, Eno1, Hsp90ab1, MSN, and Ubc) in CW008-treated MSC CM. (G) Dose responses of TT2 OS cells in response to CW008-treated MSC CM with IC 50 at 390 μg/mL. (H) Dose responses and IC 50 of TT2 OS cells in response to 5 tumor-suppressing proteins (Calr, Eno1, Hsp90ab1, MSN, and Ubc).

    Techniques Used: Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

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    Cell Signaling Technology Inc anti inflammatory regulators
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    Cell Signaling Technology Inc anti eno1 antibody
    A: Activity of immuno-captured <t>α-enolase</t> <t>(ENO1)</t> from HEK293T cells after stimulation with insulin and AKT-inhibition with CCT128930. Data represent means ± SD of n = 7 experiments. B: Detection of immuno-captured α-enolase after α-enolase activity assay. After detection of α-enolase blots were incubated with anti-pan AKT antibody. Note that AKT was also detected after isolation of α-enolase by the α-enolase antibody.
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    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) <t>Enolase</t> <t>1</t> <t>(Eno1),</t> Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
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    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) <t>Enolase</t> <t>1</t> <t>(Eno1),</t> Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
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    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) <t>Enolase</t> <t>1</t> <t>(Eno1),</t> Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).
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    A: Activity of immuno-captured α-enolase (ENO1) from HEK293T cells after stimulation with insulin and AKT-inhibition with CCT128930. Data represent means ± SD of n = 7 experiments. B: Detection of immuno-captured α-enolase after α-enolase activity assay. After detection of α-enolase blots were incubated with anti-pan AKT antibody. Note that AKT was also detected after isolation of α-enolase by the α-enolase antibody.

    Journal: PLoS ONE

    Article Title: Systematic Analysis Reveals Elongation Factor 2 and α-Enolase as Novel Interaction Partners of AKT2

    doi: 10.1371/journal.pone.0066045

    Figure Lengend Snippet: A: Activity of immuno-captured α-enolase (ENO1) from HEK293T cells after stimulation with insulin and AKT-inhibition with CCT128930. Data represent means ± SD of n = 7 experiments. B: Detection of immuno-captured α-enolase after α-enolase activity assay. After detection of α-enolase blots were incubated with anti-pan AKT antibody. Note that AKT was also detected after isolation of α-enolase by the α-enolase antibody.

    Article Snippet: Primary Antibodies (Cell Signaling Technology, abcam): AKT2 Mouse mAB (5239), eEF2-Antibody (2332), GAPDH Rabbit mAB (2118), AKT1 Mouse mAB (2967), anti-ENO1-antibody (ab85086).

    Techniques: Activity Assay, Inhibition, Incubation, Isolation

    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Article Snippet: Antibodies against c-Myc, Oct4, Sox2, Klf4, Lrp5, Runx2, Snail, TGFβ, Eno1, Eef2, vinculin, β-catenin, p-Akt, Akt, p-NFkB p65, NFkB p65, p-ERK, ERK (Cell Signaling), MMP9, NFATc1, cathepsin K (Santa Cruz, Dallas, TX, USA), TRAIL (Novus, Centennial, CO, USA), p53 (Invitrogen, Carlsbad, CA, USA), Hsp90ab1 (Abcam, Cambridge, UK), Kdm3a (Thermo Fisher Scientific) and β-actin as a control (Sigma) were employed.

    Techniques: Mass Spectrometry, Derivative Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Recombinant

    Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Article Snippet: Antibodies against c-Myc, Oct4, Sox2, Klf4, Lrp5, Runx2, Snail, TGFβ, Eno1, Eef2, vinculin, β-catenin, p-Akt, Akt, p-NFkB p65, NFkB p65, p-ERK, ERK (Cell Signaling), MMP9, NFATc1, cathepsin K (Santa Cruz, Dallas, TX, USA), TRAIL (Novus, Centennial, CO, USA), p53 (Invitrogen, Carlsbad, CA, USA), Hsp90ab1 (Abcam, Cambridge, UK), Kdm3a (Thermo Fisher Scientific) and β-actin as a control (Sigma) were employed.

    Techniques: Over Expression, Recombinant, Immunoprecipitation, Western Blot, Mutagenesis, Pull Down Assay, Negative Control, Plasmid Preparation, Transfection

    Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Article Snippet: Antibodies against c-Myc, Oct4, Sox2, Klf4, Lrp5, Runx2, Snail, TGFβ, Eno1, Eef2, vinculin, β-catenin, p-Akt, Akt, p-NFkB p65, NFkB p65, p-ERK, ERK (Cell Signaling), MMP9, NFATc1, cathepsin K (Santa Cruz, Dallas, TX, USA), TRAIL (Novus, Centennial, CO, USA), p53 (Invitrogen, Carlsbad, CA, USA), Hsp90ab1 (Abcam, Cambridge, UK), Kdm3a (Thermo Fisher Scientific) and β-actin as a control (Sigma) were employed.

    Techniques: Recombinant, Over Expression, Derivative Assay

    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Article Snippet: Western blotting was conducted using antibodies against Eno1 and CD44 (Cell Signaling).

    Techniques: Mass Spectrometry, Derivative Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Recombinant

    Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Article Snippet: Western blotting was conducted using antibodies against Eno1 and CD44 (Cell Signaling).

    Techniques: Over Expression, Recombinant, Immunoprecipitation, Western Blot, Mutagenesis, Pull Down Assay, Negative Control, Plasmid Preparation, Transfection

    Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Article Snippet: Western blotting was conducted using antibodies against Eno1 and CD44 (Cell Signaling).

    Techniques: Recombinant, Over Expression, Derivative Assay

    Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Prediction of the tumor suppressors in CM by mass spectrometry-based whole-genome proteomics. The single and double asterisks indicate p < 0.05 and 0.01, respectively. CN = control, Oct4 = Oct4 plasmids, c-Myc = c-Myc plasmids, Sox2 = Sox2 plasmids, Klf4 = Klf4 plasmids, and CM = conditioned medium. ( A ) Summary list of the potential tumor suppressors by mass spectrometry-based whole-genome proteomics. ( B ) Enolase 1 (Eno1), Hsp90ab1 (HSP), Eef2, and vinculin (VCL) as 4 tumor-suppressor candidates based on MTT-based viability. ( C ) Upregulation of Eno1, Hsp90ab1, Eef2, VCL, p53, and Trail in 4T1.2 cell-derived CM with the overexpression of Oct4, c-Myc, and the treatment with OAC2. The overexpression of Sox2 and Klf4 did not alter their levels. ( D ) Alterations in the levels of Eno1 and Hsp90ab1 in Oct4 and c-Myc CM by ELISA. ( E ) Reduction in MTT-based viability of 4T1.2 cells by the treatment with Eno1 and/or Hsp90ab1 recombinant proteins. ( F ) Tumor selectivity from the MTT-based viability of tumor cells (4T1.2 mammary tumor cells, EO771 mammary tumor cells, and MDA-MB-231 breast cancer cells) and human epithelium cells (KTB34-hTERT and KTB22-hTERT). Tumor selectivity is defined as a ratio of (MTT-based reduction in tumor cells) to (MTT-based reduction in non-tumor cells).

    Article Snippet: Protein samples were pretreated with agarose beads conjugated with protein A and rabbit IgG, followed by the overnight immunoprecipitation with the beads conjugated with anti-Eno1 antibodies (Cell Signaling).

    Techniques: Mass Spectrometry, Derivative Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Recombinant

    Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Tumor-promoting effects by the overexpression of Eno1, Eef2, and VCL in 4T1.2 mammary tumor cells, and tumor-suppressing effects by the administration of their recombinant proteins. The double asterisk indicates p < 0.01. CN = control, Eno1 = enolase 1, VCL = vinculin, and Hsp = Hsp90ab1. ( A-C ) Elevation in EdU-based proliferation, transwell invasion, and the upregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail by the overexpression of Eno1, Eef2, and VCL in 4T1.2 tumor cells. ( D ) Decrease in EdU-based proliferation by the administration of Eno1, Eef2, and VCL recombinant proteins. ( E ) Reduction in transwell invasion by the administration of Eno1, Eef2, and VCL recombinant proteins. ( F ) Downregulation of Lrp5, MMP9, Runx2, TGFβ, and Snail in 4T1.2 tumor cells by the administration of Eno1, Eef2, and VCL recombinant proteins. ( G ) Co-immunoprecipitation of CD44 by Eno1 in 4T1.2 cells. ( H-I ) Suppression of the reduction in MTT-based viability by Eno1 in response to the silencing of CD44. ( J ) Downregulation of Lrp5, Runx2, MMP9 and Snail in 4T1.2 cells by the administration of Eno1 recombinant proteins, and the suppression by the silencing of CD44. ( K-L ) Western blotting of wild-type and mutant CD44 proteins, which were pulled down by Halo-tagged Eno1 proteins. PD = pull-down assay, NC = negative control, pl = Eno1 or CD44 proteins from plasmid transfection, MT = mutant CD44 without a cytoplasmic domain, and WT = wild-type CD44.

    Article Snippet: Protein samples were pretreated with agarose beads conjugated with protein A and rabbit IgG, followed by the overnight immunoprecipitation with the beads conjugated with anti-Eno1 antibodies (Cell Signaling).

    Techniques: Over Expression, Recombinant, Immunoprecipitation, Western Blot, Mutagenesis, Pull Down Assay, Negative Control, Plasmid Preparation, Transfection

    Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Journal: Theranostics

    Article Title: Counterintuitive production of tumor-suppressive secretomes from Oct4- and c-Myc-overexpressing tumor cells and MSCs

    doi: 10.7150/thno.70549

    Figure Lengend Snippet: Downregulation of PDL-1 and Kdm3a in 4T1.2 mammary tumor cells by Hsp90ab1, Eno1, Eef2, and VCL, and the suppression of the development of osteoclasts. CN = control, Hsp = Hsp90ab1, Eno1 = enolase 1, VCL = vinculin, Oct4 = Oct4 plasmids, and CM = conditioned medium. The double asterisk indicates p < 0.01. ( A ) Reduction in the size and weight of mammary tumors by the daily intravenous administration of 1 μg/mL Eno1. EO771 mammary tumor cells were inoculated into the mammary fat pad of C57BL/6 female mice (N = 10). (B) Reduction in p-AKT, NFkB p65, p-ERK, and TNFα in 4T1.2 cells in response to Eno1 recombinant proteins. ( C ) Reduction in PDL1 in 4T1.2 cells by Oct4/cMyc-overexpressing 4T1.2 CM, and Eno1, Hsp, Eef2, and VCL recombinant proteins. ( D ) Reduction in Kdm3a in 4T1.2 cells in response to Eno1, Hsp90ab1, Eef2, and/or VCL recombinant proteins. ( E ) Elevation of Kdm3a in 4T1.2 cells by the overexpression of Eno1, Eef2, and VCL. ( F ) Suppression of RANKL-stimulated osteoclast development by Oct4-overexpressing CM. ( G ) Reduction in the levels of cathepsin K and NFATc1 in RANKL-stimulated osteoclasts by Oct4-overexpressing CM. ( H ) Regulatory mechanism by the tumor-suppressive secretomes, which were derived from Oct4- and c-Myc-overexpressing tumor cells.

    Article Snippet: Protein samples were pretreated with agarose beads conjugated with protein A and rabbit IgG, followed by the overnight immunoprecipitation with the beads conjugated with anti-Eno1 antibodies (Cell Signaling).

    Techniques: Recombinant, Over Expression, Derivative Assay