title: Enforced expression of RASAL1 suppresses cell proliferation and the             transformation ability of gastric cancer cells.
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.
authors: 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, PR China.
authors: Fengchang
authors: F
authors: Qiao
authors: Xianwei
authors: X
authors: Su
authors: Xuemei
authors: X
authors: Qiu
authors: Danwen
authors: D
authors: Qian
authors: Xiao
authors: X
authors: Peng
authors: Hong
authors: H
authors: Chen
authors: Zhujiang
authors: Z
authors: Zhao
authors: Hong
authors: H
authors: Fan
mesh_terms: D000368:Aged; D001374:Azacitidine / Q000031:analogs & derivatives / Q000494:pharmacology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000187:drug effects; D019175:DNA Methylation / Q000187:drug effects; D000077209:Decitabine; D004305:Dose-Response Relationship, Drug; D044127:Epigenesis, Genetic; D020031:Epstein-Barr Virus Infections / Q000235:genetics; D005260:Female; D020690:GTPase-Activating Proteins / Q000235:genetics* / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D016481:Helicobacter Infections / Q000235:genetics; D056572:Histone Deacetylase Inhibitors / Q000494:pharmacology; D006801:Humans; D006877:Hydroxamic Acids / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D013274:Stomach Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D020703:ras GTPase-Activating Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D020690:GTPase-Activating Proteins; D056572:Histone Deacetylase Inhibitors; D006877:Hydroxamic Acids; C580923:RASAL1 protein, human; D020703:ras GTPase-Activating Proteins; C012589:trichostatin A; D000077209:Decitabine; D001374:Azacitidine