CtIP promotes G2/M arrest in etoposide‐treated HCT116 cells in a p53‐independent manner
Acquired resistance to cytotoxic antineoplastic agents is a major clinical challenge in tumor therapy; however, the mechanisms involved are still poorly understood. In this study, we show that knockdown of CtIP, a corepressor of CtBP, promotes cell proliferation and alleviates G2/M phase arrest in e...
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| Published in | Journal of cellular physiology Vol. 234; no. 7; pp. 11871 - 11881 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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| Abstract | Acquired resistance to cytotoxic antineoplastic agents is a major clinical challenge in tumor therapy; however, the mechanisms involved are still poorly understood. In this study, we show that knockdown of CtIP, a corepressor of CtBP, promotes cell proliferation and alleviates G2/M phase arrest in etoposide (Eto)‐treated HCT116 cells. Although the expression of p21 and growth arrest and DNA damage inducible α (GADD45a), which are important targets of p53, was downregulated in CtIP‐deficient HCT116 cells, p53 deletion did not affect G2/M arrest after Eto treatment. In addition, the phosphorylation levels of Ser317 and Ser345 in Chk1 and of Ser216 in CDC25C were lower in CtIP‐deficient HCT116 cells than in control cells after Eto treatment. Our results indicate that CtIP may enhance cell sensitivity to Eto by promoting G2/M phase arrest, mainly through the ATR‐Chk1‐CDC25C pathway rather than the p53‐p21/GADD45a pathway. The expression of CtIP may be a useful biomarker for predicting the drug sensitivity of colorectal cancer cells.
CtIP can modulate the etoposide sensitivity of HCT116 cells by promoting G2/M phase arrest, which mainly through the ATR‐Chk1‐CDC25C pathway rather than the p53‐p21/GADD45a pathway. |
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| AbstractList | Abstract
Acquired resistance to cytotoxic antineoplastic agents is a major clinical challenge in tumor therapy; however, the mechanisms involved are still poorly understood. In this study, we show that knockdown of CtIP, a corepressor of CtBP, promotes cell proliferation and alleviates G2/M phase arrest in etoposide (Eto)‐treated HCT116 cells. Although the expression of p21 and growth arrest and DNA damage inducible α (GADD45a), which are important targets of p53, was downregulated in CtIP‐deficient HCT116 cells, p53 deletion did not affect G2/M arrest after Eto treatment. In addition, the phosphorylation levels of Ser317 and Ser345 in Chk1 and of Ser216 in CDC25C were lower in CtIP‐deficient HCT116 cells than in control cells after Eto treatment. Our results indicate that CtIP may enhance cell sensitivity to Eto by promoting G2/M phase arrest, mainly through the ATR‐Chk1‐CDC25C pathway rather than the p53‐p21/GADD45a pathway. The expression of CtIP may be a useful biomarker for predicting the drug sensitivity of colorectal cancer cells. Acquired resistance to cytotoxic antineoplastic agents is a major clinical challenge in tumor therapy; however, the mechanisms involved are still poorly understood. In this study, we show that knockdown of CtIP, a corepressor of CtBP, promotes cell proliferation and alleviates G2/M phase arrest in etoposide (Eto)-treated HCT116 cells. Although the expression of p21 and growth arrest and DNA damage inducible α (GADD45a), which are important targets of p53, was downregulated in CtIP-deficient HCT116 cells, p53 deletion did not affect G2/M arrest after Eto treatment. In addition, the phosphorylation levels of Ser317 and Ser345 in Chk1 and of Ser216 in CDC25C were lower in CtIP-deficient HCT116 cells than in control cells after Eto treatment. Our results indicate that CtIP may enhance cell sensitivity to Eto by promoting G2/M phase arrest, mainly through the ATR-Chk1-CDC25C pathway rather than the p53-p21/GADD45a pathway. The expression of CtIP may be a useful biomarker for predicting the drug sensitivity of colorectal cancer cells. Acquired resistance to cytotoxic antineoplastic agents is a major clinical challenge in tumor therapy; however, the mechanisms involved are still poorly understood. In this study, we show that knockdown of CtIP, a corepressor of CtBP, promotes cell proliferation and alleviates G2/M phase arrest in etoposide (Eto)‐treated HCT116 cells. Although the expression of p21 and growth arrest and DNA damage inducible α (GADD45a), which are important targets of p53, was downregulated in CtIP‐deficient HCT116 cells, p53 deletion did not affect G2/M arrest after Eto treatment. In addition, the phosphorylation levels of Ser317 and Ser345 in Chk1 and of Ser216 in CDC25C were lower in CtIP‐deficient HCT116 cells than in control cells after Eto treatment. Our results indicate that CtIP may enhance cell sensitivity to Eto by promoting G2/M phase arrest, mainly through the ATR‐Chk1‐CDC25C pathway rather than the p53‐p21/GADD45a pathway. The expression of CtIP may be a useful biomarker for predicting the drug sensitivity of colorectal cancer cells. CtIP can modulate the etoposide sensitivity of HCT116 cells by promoting G2/M phase arrest, which mainly through the ATR‐Chk1‐CDC25C pathway rather than the p53‐p21/GADD45a pathway. |
| Author | Qi, Wenjing Liu, Wenguang Wang, Ruoxi Chen, Dandan Wang, Hailong Ke, Yueshuang Chen, Hongyu Shan, Jin Zeng, Xianlu |
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| SubjectTerms | Antineoplastic Agents - pharmacology Antineoplastic drugs Apoptosis - drug effects Biomarkers Cell Cycle Proteins - drug effects Cell Cycle Proteins - metabolism Cell Line, Tumor Cell proliferation CHK1 protein Clonal deletion Colorectal cancer Colorectal carcinoma CtIP Cyclin-dependent kinase inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - drug effects Cyclin-Dependent Kinase Inhibitor p21 - metabolism Cytotoxicity Deoxyribonucleic acid DNA DNA damage DNA Damage - drug effects drug sensitivity Endodeoxyribonucleases - metabolism Etoposide Etoposide - pharmacology G2 Phase Cell Cycle Checkpoints - drug effects G2/M phase arrest Gadd45A protein Gene expression HCT116 Cells Humans M Phase Cell Cycle Checkpoints - drug effects p53 p53 Protein Phosphorylation Sensitivity enhancement Signal Transduction - drug effects Tumor Suppressor Protein p53 - drug effects Tumor Suppressor Protein p53 - genetics |
| Title | CtIP promotes G2/M arrest in etoposide‐treated HCT116 cells in a p53‐independent manner |
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