Author/Authors :
Lai، نويسنده , , Rai-Hua and Hsiao، نويسنده , , Ya-Wen and Wang، نويسنده , , Mei-Jung and Lin، نويسنده , , Huan-Yu and Wu، نويسنده , , Chew-Wun and Chi، نويسنده , , Chin-Wen and Li، نويسنده , , Anna Fen-Yau and Jou، نويسنده , , Yuh-Shan and Chen، نويسنده , , Jeou-Yuan Chen، نويسنده ,
Abstract :
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.
Keywords :
Loss of Heterozygosity , SOCS6 , Gastric cancer , Promoter hypermethylation , apoptosis , Growth suppression