Loss of expression of wtKLF6 in hepatocellular carcinoma and its effect on hepatocellular carcinoma cell proliferation
10.3760/cma.j.issn.1007-8118.2011.02.014
- VernacularTitle:KLF6在肝细胞癌中的表达缺失及其对肝癌细胞增殖的影响
- Author:
Shaoping WANG
;
Lili KANG
;
Xiaoping CHEN
;
Hejun ZHOU
;
Yujun SUI
;
Wenzhang SI
- Publication Type:Journal Article
- Keywords:
Carcinoma,hepatocellular;
Tumor suppressor gene;
Kruppel-like factor 6;
Gene expression;
Cell proliferation
- From:
Chinese Journal of Hepatobiliary Surgery
2011;17(2):132-137
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression and genetic alterations of KLF6 in hepatocellular carcinoma (HCC) and explore their functional mechanisms in the oncogenesis and development of HCC. Methods Real-time quantitative-PCR, direct sequencing and LOH approaches were used to detect KLF6 genetic abnormalities in HCC. The experiment had 2 groups, an experimental group and a control group. In the experimental group, the transfected plasmid pcDNA3.0 was recombined with KLF6 and tranfected into HCC HepG2 cells. MTT, flow cytometry and Western blotting were used to observe the effect of anti-oncogene wild type KLF6 on HepG2 cells by transgenic method for 48 h.Results Expression levels of KLF6 were significantly downregulated in HCCs(P＜0. 01), as detected by qRT-PCR. LOH occurred in 11 (52%) of the 21 tumors, and all the samples with LOH showed KLF6 down-regulation. The mutational frequency was 29%, and sequence changes located in activation domain of KLF6. Meanwhile, MTT assay showed a significant antiproliferative effect of the transfected wtKLF6 on HepG2 cells(42.7%, P＜0.05). Fluorescence-activated cell sorting analysis revealed that KLF6 induced apoptosis. Conclusion The deregulation of KLF6 together with genetic abnormalities of allelic imbalance and mutations may play an important role in HCC pathogenesis.
