1. COPB2 gene silencing inhibits colorectal cancer cell proliferation and induces apoptosis via the JNK/c-Jun signaling pathway.
- Author
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Wang Y, Xie G, Li M, Du J, and Wang M
- Subjects
- Cell Line, Tumor, Cell Movement drug effects, Cell Proliferation drug effects, Cell Survival drug effects, Coatomer Protein antagonists & inhibitors, Colorectal Neoplasms drug therapy, Colorectal Neoplasms metabolism, Gene Expression Regulation, Neoplastic drug effects, Gene Silencing, HCT116 Cells, HT29 Cells, Humans, MAP Kinase Signaling System, Proto-Oncogene Proteins c-jun metabolism, Survival Analysis, Coatomer Protein genetics, Colorectal Neoplasms genetics, RNA, Small Interfering pharmacology, Up-Regulation drug effects
- Abstract
Objectives: Colorectal cancer (CRC) is one of the most common malignant human tumors. It is associated with high morbidity and mortality rates. In recent years, tumor gene therapy has emerged as a promising new approach for colorectal cancer therapy. Herein, we identify and analyze the role of COPB2 (coatomer protein complex, subunit beta 2) in proliferation and apoptosis of CRC cells., Methods: To investigate the role of COPB2 in the proliferation and apoptosis of CRC cells, a shCOPB2 vector and a shCtrl vector were constructed for transfection into RKO and HCT116 cells. Cells proliferation was subsequently measured via cell counting kit-8 (CCK8) assay and Celigo cell counting assay. Apoptosis was measured via flow cytometry. The activity level of Caspase 3/7 was measured. Finally, the level of several JNK/c-Jun apoptosis pathway-related proteins were measured to characterize the mechanism of apoptosis., Results: Our results showed that the proliferation rate was decreased and the apoptosis rate was increased in shCOPB2-treated RKO and HCT116 cells compared to those in controls. After the silencing of COPB2, JNK/c-Jun signal pathway activation was increased, the expression levels of apoptosis pathway-related proteins, such as Bad, p53 and Caspase 3, were also increased., Conclusion: COPB2 gene silencing can inhibit RKO and HCT116 cells proliferation and induce apoptosis via the JNK/c-Jun signaling pathway., Competing Interests: NO authors have competing interests.
- Published
- 2020
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