SOCS6, down-regulated in gastric cancer, inhibits cell proliferation and colony formation

被引：57

作者：

Lai, Rai-Hua ^{[2
]}

Hsiao, Ya-Wen ^{[1
]}

Wang, Mei-Jung ^{[1
]}

Lin, Huan-Yu ^{[3
]}

Wu, Chew-Wun ^{[4
]}

Chi, Chin-Wen ^{[2
,5
]}

Li, Anna Fen-Yau ^{[6
]}

Jou, Yuh-Shan ^{[1
]}

Chen, Jeou-Yuan ^{[1
,7
]}

机构：

[1] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan

[2] Natl Yang Ming Univ, Inst Pharmacol, Taipei 112, Taiwan

[3] Natl Yang Ming Univ, Inst Biochem & Mol Biol, Taipei 112, Taiwan

[4] Taipei Vet Gen Hosp, Dept Surg, Taipei, Taiwan

[5] Taipei Vet Gen Hosp, Dept Med Res & Educ, Taipei, Taiwan

[6] Taipei Vet Gen Hosp, Dept Pathol, Taipei, Taiwan

[7] Natl Yang Ming Univ, Inst Genome Sci, Taipei 112, Taiwan

来源：

CANCER LETTERS | 2010年 / 288卷 / 01期

关键词：

SOCS6; Gastric cancer; Loss of heterozygosity; Promoter hypermethylation; Growth suppression; Apoptosis; CYTOKINE SIGNALING-1; CHROMOSOME; 18Q; ABERRANT METHYLATION; NEGATIVE REGULATOR; JAK/STAT PATHWAY; INSULIN-RECEPTOR; BREAST-CANCER; GROWTH; GENE; HYPERMETHYLATION;

D O I：

10.1016/j.canlet.2009.06.025

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Members of the suppressor of cytokine-induced signaling (SOCS) family are negative regulators of cytokine signaling pathways. By mRNA differential display, we showed that SOCS6 was frequently down-regulated in gastric cancer (GC). Our data showed that allelic loss and promoter hypermethylation may account for the major mechanisms leading to SOCS6 inactivation. Ectopic expression of SOCS6 suppressed cell growth and colony formation, in part through eliciting intrinsic apoptotic pathway, accompanied with decreased mitochondrial membrane potential. Taken together, this study provides molecular and functional data supporting the importance of loss-of-function of SOCS6 as a frequent event in gastric tumorigenesis. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：75 / 85

页数：11

共 36 条

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