Abstract
ABSTRACTThe inhibitory effect of buforin IIb on different types of cancer, although not liver cancer, has been demonstrated previously. The aim of the present study was to investigate the effects of buforin IIb on the progression of liver cancer. The human liver cancer cell line HepG2 was treated with purified buforin IIb and the cell activity was determined by MTT, colony formation and transwell assays. The protein expression levels of cyclin-dependent kinases (CDKs) and cyclins were analyzed by western blotting and immunofluorescent cell staining. A tumor growth model was constructed using nude mice, and buforin IIb treatment was administered. The levels of CDK2 and cyclin A in the tumor tissues were detected by western blotting. Buforin IIb treatment depressed cell viability and colony formation and induced apoptosis significantly, and 1.0 µM concentration of buforin IIb was found to be the optimal dosage. The cell cycle was arrested at the G2/M phase following buforin IIb treatment. CDK2 and cyclin A were downregulated by treatment of the cells with 1.0 µM buforin IIb for 24 h. Treatment with buforin IIb also inhibited the migration of liver cancer cells in vitro. Furthermore, 50 nmol buforin IIb injection suppressed HepG2 cell subcutaneous tumor growth in the nude mouse model. Similar to the in vitro results, buforin IIb injection reduced the expression of CDK2 and cyclin A in the tumor tissue. these results demonstrate that buforin IIb inhibited liver cancer cell growth via the regulation of CDK2 and cyclin A expression.
Highlights
Metastatic liver tumors represent the most prevalent cancers in adults (Bosch et al 2004)
Cell cycle analysis indicated that the cells were significantly arrested at the G2/M phase following buforin IIb treatment compared with the control (Figure 1(F))
These results suggested that buforin IIb inhibits cell proliferation and promote apoptosis in liver cancer
Summary
Metastatic liver tumors represent the most prevalent cancers in adults (Bosch et al 2004). As a leading cause of morbidity and mortality worldwide, liver cancer affects survival and the quality of life (Bosch et al 2004). Resection surgery, radiation therapy and chemotherapy are the standard treatments used for patients with liver cancer (Baskar et al 2012). Severe side effects arise following radiation therapy and chemotherapy (Lawrence et al 1995; Wulf et al 2006). These treatments have shown limited curative effects and poor prognosis in clinical practice (Bruix and Sherman 2011). The development of novel agents that target liver cancer is, urgently required to improve the treatment of liver cancer
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