Enforced expression of RASAL1 suppresses cell proliferation and the transformation ability of gastric cancer cells

Qiao,Fengchang; Su,Xianwei; Qiu,Xuemei; Qian,Danwen; Peng,Xiao; Chen,Hong; Zhao,Zhujiang; Fan,Hong

doi:10.3892/or.2012.1920

Enforced expression of RASAL1 suppresses cell proliferation and the transformation ability of gastric cancer cells

Authors:
- Fengchang Qiao
- Xianwei Su
- Xuemei Qiu
- Danwen Qian
- Xiao Peng
- Hong Chen
- Zhujiang Zhao
- Hong Fan
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Affiliations: Key Laboratory of Developmental Genes and Human Diseases, Ministry of Education, Institute of Life Science, and Department of Genetics and Developmental Biology, Medical School of Southeast University, Nanjing 210009, P.R. China, Zhong Da Hospital, Medical School of Southeast University, Nanjing 210009, P.R. China
Published online on: July 19, 2012 https://doi.org/10.3892/or.2012.1920
Pages: 1475-1481

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Abstract

RAS protein activator like 1 (RASAL1) is a member of the RAS GTPase-activating protein (GAP) family, and it is an important molecule in the regulation of RAS activation. In the present study, we investigated the role of RASAL1 in gastric carcinogenesis. Decreased expression pattern of RASAL1 in gastric cancer tissues and cell lines was found in protein and RNA levels, although there was no statistically significant relationship between RASAL1 and clinicopathological features. Restored expression of RASAL1 induced by DNA methylation inhibitor 5-aza-2'-deoxycytidine (5'-AZA) and HDAC inhibitor trichostatin A (TSA) implied that RASAL1 expression is regulated by epigenetic mechanisms. The biological role of RASAL1 in gastric carcinogenesis was determined by in vitro tumorigenicity assays. Overexpression of RASAL1 showed suppression of cell proliferation due to cell apoptosis. Subsequently, enforced expression of RASAL1 repressed significantly the gastric cancer cell transformation ability. These findings demonstrated that decreased RASAL1 expression is a characteristic of gastric cancer and regulated by epigenetic mechanisms. RASAL1 may be a functional tumor suppressor involved in gastric cancer. This study provides novel insights into the biological role of RASAL1 in gastric carcinogenesis.

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