Gastric Cancer
Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 15, 2002; 8(4): 580-585
Published online Aug 15, 2002. doi: 10.3748/wjg.v8.i4.580
Profiling of differentially expressed genes in human Gastric carcinoma by cDNA expression array
Lian-Xin Liu, Zhi-Hua Liu, Hong-Chi Jiang, Xin Qu, Wei-Hui Zhang, Lin-Feng Wu, An-Long Zhu, Xiu-Qin Wang, Min Wu
Lian-Xin Liu, Hong-Chi Jiang, Xin Qu, Wei-Hui Zhang, Lin-Feng Wu, An-Long Zhu, Department of Surgery, the First Clinical College, Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Lian-Xin Liu, Zhi-Hua Liu, Xiu-Qin Wang, Min Wu, National Laboratory of Molecular Oncology, Department of Cell Biology, Cancer Institute, Chinese Academy of Medical Science & Peking Union Medical College, Beijing 100021, China
Author contributions: All authors contributed equally to the work.
Supported by China Key Program on Basic Research, Grant Number: Z19-01-01-02; Chinese Climbing Project No.18; Youth Natural Scientific Foundation of Heilongjiang Province
Correspondence to: Dr. Lian-Xin Liu, Department of Surgery, the First Clinical College, Harbin Medical University, No.23 Youzheng Street, Nangang District, Harbin 150001, Heilongjiang Province, China.
Telephone: +86-451-3668999 Fax: +86-451-3670428
Received: July 8, 2002
Revised: July 15, 2002
Accepted: July 19, 2002
Published online: August 15, 2002

AIM: To investigate the expression of cancer related genes in gastric carcinoma (GC) through the use of Atlas Human Cancer Array membranes with 588 well-characterized human genes related to cancer and tumor biology.

METHODS: Hybridization of cDNA blotting membrane was performed with 32P-labeled cDNA probes synthesized from RNA isolated from gastric carcinoma and adjacent noncancerous gastric epithelial tissue. AtlasImage, which is a software specific to array, was used to analyze the result.

RESULTS: The differentially expression cell cycle/growth regulator in GC showed a stronger tendency toward cell proliferation with 2.7-fold up-regulation of CK1. The promoter genes of apoptosis were down-regulated, including caspase-8 precursor, caspase-9 and caspase-10. Among the oncogene/tumor suppressor genes, ABL2 was down-regulated. In addition, some genes were up-regulated, including matrix metalloproteinse 2 (MMP-2), MMP-16 (MT3-MMP), SKY, CD9 and semaphorin V. A number of genes were down-regulated, including neuroendocrine-dlg (NE-dlg), retinoic acid receptor gamma and tumor suppressor DCC colorectal. In general, The expression of the cancer progression genes were up-regulated, while the expression of anti-cancer progression genes were down-regulated.

CONCLUSION: Investigation of these genes should help to disclose the molecular mechanism of the onset, progression and prognosis of GC. Several genes are reported herein to be altered in GC for the first time. The quick and high-throughout method of profiling gene expression by cDNA array provides us with an overview of key factors that may involved in GC, and may aid the study of GC carcinogenesis and provide molecular targets for diagnosis and therapy. The precise relationship between the altered genes and gastric carcinogenesis is a matter for further investigation.

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