JIB‑04 induces cell apoptosis via activation of the p53/Bcl‑2/caspase pathway in MHCC97H and HepG2 cells
| Autor: | De Cai, Yongxin Yin, Huang Xiaojie, Mingyi Li, Bin Liu, Runzhi Zhu, Jie Liu, Liao Weiguo |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Cancer Research Lung Neoplasms Cell Survival Cell Aminopyridines 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cell Line Tumor medicine Humans Viability assay Caspase Cell Proliferation biology Dose-Response Relationship Drug Chemistry Hydrazones Prostatic Neoplasms General Medicine Hep G2 Cells Cell cycle Pifithrin Gene Expression Regulation Neoplastic 030104 developmental biology medicine.anatomical_structure Oncology Proto-Oncogene Proteins c-bcl-2 Apoptosis Cell culture 030220 oncology & carcinogenesis Caspases biology.protein Cancer research Signal transduction Tumor Suppressor Protein p53 Signal Transduction |
| Zdroj: | Oncology reports. 40(6) |
| ISSN: | 1791-2431 |
| Popis: | JIB‑04 is a structurally unique small molecule, known to exhibit anticancer activity and to inhibit the growth of human lung cancer and prostate cancer cell lines. However, the anticancer effect of JIB‑04 against human hepatic carcinoma, and its underlying mechanisms, are still unclear. In the present study, MHCC97H and HepG2 cells were employed to investigate the anticancer effects of JIB‑04 on cell viability and apoptosis. Annexin V/PI staining, a CCK‑8 assay and western blot analysis demonstrated that JIB‑04 induced apoptosis in MHCC97H and HepG2 cells, which was evidenced by the expression of proapoptotic and apoptotic proteins including p53, Bak, Bax, caspase‑3 and caspase‑9. Subsequently, the expression trends of Bcl‑2 and p53 were reversed after co‑treatment with pifithrin‑α (PFT‑α, a p53 inhibitor). The results revealed that JIB‑04 suppressed the cell viability of MHCC97H and HepG2 cells in a concentration‑dependent manner. Meanwhile, it was also demonstrated that JIB‑04 effectively triggered MHCC97H and HepG2 cell apoptosis by downregulating Bcl‑2/Bax expression, and upregulating proapoptotic and apoptotic protein expression via the p53/Bcl2/caspase signaling pathway. JIB‑04 had effects on the inhibition of cell viability and the induction of apoptosis in MHCC97H and HepG2 cells. The underlying mechanism of action of JIB‑04 was associated with the p53/Bcl‑2/caspase signaling pathway. Our findings provide a foundation for understanding the anticancer effect of JIB‑04 on MHCC97H and HepG2 cells, and suggested that JIB‑04 may be a promising therapeutic agent in human liver cancer. |
| Databáze: | OpenAIRE |
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