The Role of CHMP4C on Proliferation in the Human Lung Cancer A549 Cells ()
ABSTRACT
The human lung
cancer
has high incidence
rate and mortality among the carcinoma. The research on enhancing the efficacy
of therapy for lung cancer is significant. A resent research found that as a
subunit of ESCRT-III, CHMP4C functioned to retard
abscission timing to coordinate midbody resolution and prevent accumulation of
DNA damage in the abscission checkpoint through phosphorylated by AuroraB. In the current study, we evaluated the possible
mechanism of the effects of CHMP4C inhibition on cell cycle and cell survival
in A549 cells. We found that CHMP4C knockdown caused lagging S phase in cell cycle through enhancing the phosphorylation
of Rb, raising the expression of cyclin B1-cdc2 and suppressing the activation
of cyclin A. Meanwhile, CHMP4Cdeletion depressed cell survival via decreasing cell viability and increasing caspase 3/7 activity. This study
may promote new significant reference and advance for the mechanism underlying
specific function of CHMP4C as well as further research on enhancing therapy
effect on non-small lung cancer.
Share and Cite:
Li, K. , Liu, J. , Tian, M. , Piao, C. , Ruan, J. , Gao, L. , Qi, X. , Gao, G. and Su, X. (2015) The Role of CHMP4C on Proliferation in the Human Lung Cancer A549 Cells.
Journal of Cancer Therapy,
6, 1223-1228. doi:
10.4236/jct.2015.615133.