Open AccessNidus vespae protein inhibiting proliferation of HepG2 hepatoma cells through extracellular signal‐regulated kinase signaling pathways and inducing G 1 cell cycle arrest
Author(s) -
Wang Changdong,
Chen Peng,
Jin Hongjuan,
Yan Xu,
Gan Lu,
Li Yi,
Zhou Shiyi,
Chang Junli,
Wang Yuesheng,
Yang Guangxiao,
He Guangyuan
Publication year - 2008
Publication title -
acta biochimica et biophysica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.771
H-Index - 57
eISSN - 1745-7270
pISSN - 1672-9145
DOI - 10.1111/j.1745-7270.2008.00476.x
Subject(s) - mapk/erk pathway , signal transduction , protein kinase a , cell growth , kinase , extracellular , apoptosis , microbiology and biotechnology , cell cycle , biology , chemistry , biochemistry
A protein named NVP(1) was isolated from Nidus vespae. T he aim of the present study was to elucidate whether and how NVP(1) modulates the proliferation of HepG2 cells. NVP(1) at a concentration of 6.6 μg/ml could arrest the cell cycle at stage G 1 and inhibit the mRNA expression of cyclinB, cyclinD1 and cyclinE. NVP(1) suppressed cdk2 protein expression, but increased p27 and p21 protein expression. However, NVP(1) did not alter p16 protein expression levels. NVP(1) promoted apoptosis in HepG2 cells as indicated by nuclear chromatin condensation, and in addition, the extracellular signal‐regulated kinase (ERK) signaling pathway was activated. Moreover, the p‐ERK protein expression level was attenuated when the HepG2 cells were pretreated with ERK inhibitor PD98059. These results demonstrate that NVP(1) inhibits proliferation of HepG2 through ERK signaling pathway. NVP(1) could be a potential drug for liver cancer.