[The inhibition effect and its molecular mechanism of human cervical cancer oncogene siRNA on hepatocarcinoma cells].
OBJECTIVE
To evaluate the effect and the possible mechanism of HCCR siRNA on cell proliferation and apoptosis of hepatocarcinoma cells.


METHODS
pRIV2-siHCCR plasmids, which express small interfering RNA of HCCR were constructed and transfected into HepG2 cells. The mRNA and protein expressions of HCCR were detected by real time PCR and Western blot. The proteins p15, p16, p27, p53, and PTEN were detected by Western blot. The cell proliferation and apoptosis were observed by MTT and FACS.


RESULTS
The plasmid pRIV2-siHCCR was constructed successfully. Real time PCR and Western blot analysis showed that the HCCR siRNA effectively inhibited HCCR expression in HepG2 cells after pRIV2-siHCCR transfection. MTT method confirmed that HepG2 cell proliferation was suspended, while the cell apoptosis was increased much more than that in the control group. After the transfection with the plasmid of pRIV2-siHCCR into HepG2 cells, the expression of p53 protein was decreased, and P15 increased; and levels of PTEN, p16, and p27 were evidently not changed.


CONCLUSIONS
After being transfected with HCCR siRNA expression plasmid, the cell proliferation of HepG2 was arrested, while the apoptosis of HepG2 cells increased. Our results demonstrate the potential role of p53 and p15 in HCCR signaling.
Yang
Yan
Y
Experimental Medical Research Center, Division of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Zhou
Xue-Feng
XF
Liu
An-Ding
AD