Growth inhibition and apoptosis induced by 6-fluoro-3-formylchromone in hepatocellular carcinoma
- Equal contributors
Department of General Surgery, Changhai Hospital, No.168 Changhai Road, Shanghai, Yangpu District 200433, China
BMC Gastroenterology 2014, 14:62 doi:10.1186/1471-230X-14-62Published: 3 April 2014
Hepatocellular carcinoma (HCC) is one of the most lethal and prevalent cancers in human population. The 6-fluoro-3-formylchromone (FCC) has been shown to have anti-tumor activity against various tumor cells. However, the effects of FCC on HCC cell lines have not yet been reported. This study aims to research the effects of FCC on HCC and advance the understanding of the molecular mechanism.
HCC cell line SMMC-7721 was treated with FCC at various concentrations (0, 2, 5, 10, and 20 μg/ml) for 24, 48 and 72 h, respectively. The proliferations of SMMC-7721 cells were measured by MTT assays. After cultured 24 hours, cell cycle distribution and apoptosis were determined by flow cytometry. However, the expression levels of PCNA, Bax and Bcl-2 were measured by western blotting after 48 hours.
FCC displayed a dose- and time-dependent inhibition of the SMMC-7721 cell proliferations in vitro. It also induced apoptosis with 45.4% and caused cell accumulation in G0/G1 phase with 21.5%. PCNA and Bcl-2 expression was significantly suppressed by FCC in a dose-dependent manner (P < 0.05), while Bax expression was increased.
FCC could significantly inhibit HCC cell growth in vitro through cell cycle arrest and inducing apoptosis by suppressing PCNA expression and modulating the Bax/Bcl-2 ratio.