Published online Feb 7, 2015. doi: 10.3748/wjg.v21.i5.1498
Peer-review started: May 8, 2014
First decision: June 27, 2014
Revised: July 4, 2014
Accepted: September 19, 2014
Article in press: September 19, 2014
Published online: February 7, 2015
Processing time: 277 Days and 21.7 Hours
AIM: To observe the effect of vincristine on hepatitis B virus (HBV) replication in vitro and to study its possible mechanisms.
METHODS: Vincristine was added to the cultures of two cell lines stably expressing HBV. Then, the levels of hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and hepatitis B core antigen (HBcAg) in the supernatants or cytoplasm were examined using by enzyme-linked immunosorbent assay and Western blot. The HBV pregenome RNA (pgRNA) was detected using reverse transcription-PCR and real-time fluorescent quantitative PCR (RT-qPCR), and viral DNA was detected using Southern blot and RT-qPCR. Cell proliferation after drug treatment was detected using the BrdU incorporation test and the trypan blue exclusion assay. Cell cycle and cell apoptosis were examined using flow cytometry and Western blot.
RESULTS: Vincristine up-regulated HBV replication directly in vitro in a dose-dependent manner, and 24-h exposure to 0.1 μmol/L vincristine induced more than 4-fold and 3-fold increases in intracellular HBV DNA and the secretion of viral DNA, respectively. The expression of HBV pgRNA, intracellular HBsAg and HBcAg, and the secretion of HBeAg were also increased significantly after drug treatment. Most importantly, vincristine promoted the cell excretion of HBV nucleocapsids instead of HBV Dane particles, and the nucleocapsids are closely related to the HBV pathogenesis. Furthermore, vincristine inhibited the proliferation of cells stably expressing HBV. The higher the concentration of the drug, the more significant the inhibition of the cell proliferation and the stronger the HBV replication ability in cells. Flow cytometry indicated that cell cycle arrest at S-phase was responsible for the cell proliferation inhibition.
CONCLUSION: Vincristine has a strong stimulatory effect on HBV replication and induces cell cycle arrest, and cell proliferation inhibition may be conducive to viral replication.
Core tip: Hepatitis B virus (HBV) reactivation is an emerging clinical challenge for HBV carriers receiving anti-cancer chemotherapy. However, the mechanism for the sharp increase in viral replication in the early stages of chemotherapy is still unclear. In this research, we found that vincristine, which is a cytotoxic drug, had a direct stimulatory effect on HBV replication without the involvement of immune factors and that vincristine induced cell cycle arrest; cell proliferation inhibition may be conducive to viral replication, and this may be a novel mechanism of HBV reactivation following cytotoxic chemotherapy.