[Ectopic expression of cyclin G2 inhibits cell proliferation in HeLa cancer cell line].
OBJECTIVE
Cyclins are important proteins in cell cycle machinery, acting as positive regulators in cell proliferation. Cyclin G2 may exceptionally be a negative regulator since its expression could be induced by DNA damage and the VHL tumor suppressor protein. Furthermore, down-regulated cyclin G2 was detected in oral squamous cell carcinomas. The current study was aimed at clarifying the effects of cyclin G2 transgene expression on proliferation of cancer cells in vitro.


METHODS
Cyclin G2 cDNA was synthesized by reverse transcription-polymerase chain reaction (RT-PCR) and inserted into the pIRESneo vector at BamH I and BstX I sites to generate the recombinant plasmid pIRES-G2. The pIRES-G2 and pIRESneo plasmids were then individually introduced into HeLa cancer cell line through lipofectamine mediated transfection. After two weeks' selection in culture medium containing G418, the number of colonies was counted and the transfectant cells were morphologically observed.


RESULTS
The colony-forming efficiency of the cells transfected with pIRES-G2 construct was much lower compared with that with the control parental vector pIRESneo. The colony numbers were 76.7 +/- 24.8 and 18 +/- 10.4 in control and experimental groups, respectively, with a colony forming rate of 23.4% in the pIRES-G2 group. Furthermore, pIRES-G2 transfected cells showed a senescent morphology.


CONCLUSIONS
Ectopic overexpression of cyclin G2 in cancer cell line HeLa could inhibit cell proliferation significantly.
Tian
Yu-lou
YL
Department of Cell Biology, China Medical University, Shenyang 110001, P. R. China.
Liu
Fu-rong
FR
Liu
Jie
J
Jiang
Li
L
Luo
Yang
Y
Zhang
Xue
X
D002455:Cell Division; D003001:Cloning, Molecular; D056767:Cyclin G2; D016213:Cyclins / Q000235:genetics*; D018076:DNA, Complementary; D015870:Gene Expression; D005822:Genetic Vectors; D006367:HeLa Cells; D006801:Humans
C101593:CCNG2 protein, human; D056767:Cyclin G2; D016213:Cyclins; D018076:DNA, Complementary