Open AccessOverexpression of Cyclin L2 Inhibits Growth and Enhances Chemosensitivity in Human Gastric Cancer Cells
Author(s) -
Hong Li Li,
Huang Ding,
Ting Deng,
Li Zhou,
Xia Wang,
Ming Bai,
Yi Ba
Publication year - 2012
Publication title -
asian pacific journal of cancer prevention
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.512
H-Index - 75
eISSN - 2476-762X
pISSN - 1513-7368
DOI - 10.7314/apjcp.2012.13.4.1425
Subject(s) - survivin , cyclin b , cell cycle , cancer research , cyclin a , cyclin d , cell growth , cyclin , cyclin d1 , cyclin e1 , cyclin e , cell cycle checkpoint , apoptosis , transfection , cyclin b1 , cyclin a2 , cancer cell , biology , microbiology and biotechnology , chemistry , cancer , cell culture , cyclin dependent kinase 1 , biochemistry , genetics
Cyclin L2 is a novel member of the cyclin family, recently implicated in the regulation of cell cycle progression and/or transcriptional regulation. The present study was undertaken to investigate the effects of overexpression on tumor cell growth and chemosensitivity in human gastric cells in vitro. Cyclin L2 was transfected into human gastric cancer cell line BCG823 and expressed with a mammalian expression vector pcDNA3.1. The effects and mechanisms of cyclin L2 on cell growth, cell cycling and apoptosis were studied. Compared to control vectors, overexpression of cyclin L2 inhibited the growth of BCG823 cells and enhance their chemosensitivity to fluorouracil, docetaxel and cisplatin. The anti-proliferative effects of cyclin L2 could be due to G0/G1 arrest and apoptosis. Cyclin L2 induced G0/G1 arrest and apoptosis involved upregulation of caspase-3 and down regulation Bcl-2 and survivin. The results indicated that overexpression of cyclin L2 protein may promote efficient growth inhibition and enhance chemosensitivity to chemotherapeutic agents in human gastric cancer cells by inducing G0/G1 cell cycle arrest and apoptosis.