Liver Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 1, 2004; 10(9): 1286-1291
Published online May 1, 2004. doi: 10.3748/wjg.v10.i9.1286
Differential gene expression in human hepatocellular carcinoma Hep3B cells induced by apoptosis-related gene BNIPL-2
Li Xie, Wen-Xin Qin, Xiang-Huo He, Hui-Qun Shu, Gen-Fu Yao, Da-Fang Wan, Jian-Ren Gu
Li Xie, Wen-Xin Qin, Xiang-Huo He, Hui-Qun Shu, Gen-Fu Yao, Da-Fang Wan, Jian-Ren Gu, National Laboratory for Oncogenes and Related Genes, Shanghai Cancer Institute, Shanghai 200032, China
Wen-Xin Qin, Da-Fang Wan, Jian-Ren Gu, Cancer Institute, Shanghai Jiaotong University, Shanghai 200032, China
Author contributions: All authors contributed equally to the work.
Supported by a grant from the National Key Basic Research Program (973) of China, No. 2002CB513100 and grants from the National 863 High Technology Research and Development Program of China, No. 2001AA221141, 2002BA711A02, and 2001AA227121
Correspondence to: Dr. Wen-Xin Qin, National Laboratory for Oncogenes and Related Genes, Shanghai Cancer Institute, Shanghai Jiaotong University, Shanghai 200032, China. nlorg@public.sta.net.cn
Telephone: +86-21-64177401 Fax: +86-21-64177401
Received: September 6, 2003
Revised: October 2, 2003
Accepted: October 27, 2003
Published online: May 1, 2004
Abstract

AIM: Bcl-2/adenovirus E1B 19 ku interacting protein 2-like (BNIPL-2) is a novel protein recently identified in our laboratory. BNIPL-2 is homologous to human BNIP-2, a potentially proapoptotic protein, and can interact with Bcl-2 and Cdc42GAP and promote apoptosis in BEL-7402 cells. Here we report the gene-expression profile regulated by BNIPL-2 in human hepatocarcinoma Hep3B cells and the analysis of its potential roles in cell apoptosis.

METHODS: BNIPL-2 was overexpressed in Hep3B cells using tetracycline inducible or Tet-on system. Screened by Western blot, the cells with low background and high induction fold of BNIPL-2 were obtained. We performed Atlas human cDNA expression array hybridization on these cells and analyzed the data with Quantarray® software to identify BNIPL-2-regulated genes and their expression profile. RT-PCR was used to confirm the altered expression level of part of genes identified by the Atlas array hybridization.

RESULTS: Fifteen of 588 genes spotted on the Atlas membrane showed altered expression levels in BNIPL-2-transfected Hep3B-Tet-on cells, in which 8 genes involved in cell apoptosis or growth inhibition were up-regulated and 7 genes involved in cellular proliferation were down-regulated following overexpression of BNIPL-2.

CONCLUSION: cDNA array is a powerful tool to explore gene expression profiles under inducible conditions. The data obtained using the cDNA expression microarray technology indicates that BNIPL-2 may play its roles in apoptosis through regulating the expression of genes associated with cell apoptosis, growth inhibition and cell proliferation.

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