title: Aplasia ras homolog member I is downregulated in gastric cancer and silencing its expression promotes cell growth in vitro.
abstract: OBJECTIVE
  Aplasia ras homolog member I (ARHI) is a maternally imprinted tumor suppressor gene. ARHI protein is widely expressed in many types of human tissues; however, its expression is frequently reduced or absent in various tumors and plays a tumor suppressor role for in vitro study. In this study, we investigated the expression level of ARHI in gastric cancer in order to investigate the function of ARHI and signaling pathways that might be linked during gastric cancer development.
  
  
  METHODS
  ARHI mRNA and protein expression levels were analyzed in primary gastric cancer tissues, adjacent noncancerous gastric tissues and gastric cancer cell lines using semi-quantitative polymerase chain reaction, western blotting and immunohistochemistry, respectively.
  
  
  RESULTS
  Our results showed that both mRNA and protein expression levels of the ARHI gene were significantly downregulated (P < 0.05) in gastric cancer tissues and cell lines compared to the corresponding normal control groups. The protein expression level of ARHI was not associated with age, gender, location of tumor, tumor size or metastasis in patients with gastric cancer. However, a significant correlation between the level of ARHI protein expression and the degree of tumor differentiation and Tumor-Node-Metastasis stage was observed (P < 0.05). Furthermore, results of the methyl thiazolyl tetrazolium and Transwell assays and flow cytometric analysis showed increased cell proliferation, migration and anti-apoptotic capacities in the well-differentiated gastric cancer MKN-28 cell line, which has stably silenced ARHI protein expression.
  
  
  CONCLUSIONS
  Our data indicate that ARHI expression is downregulated in human gastric cancer and it may be a novel tumor suppressive target for gastric cancer therapy.
authors.affiliation: Department of Gastroenterology, Zhongshan Hospital affiliated with Xiamen University, Fujian Province, China.
authors.forename: Hai-Ling
authors.initials: HL
authors.lastname: Tang
authors.forename: Yi-Qun
authors.initials: YQ
authors.lastname: Hu
authors.forename: Xing-Ping
authors.initials: XP
authors.lastname: Qin
authors.forename: Amarsanaa
authors.initials: A
authors.lastname: Jazag
authors.forename: Hong
authors.initials: H
authors.lastname: Yang
authors.forename: Yi-Xuan
authors.initials: YX
authors.lastname: Yang
authors.forename: Xiao-Ning
authors.initials: XN
authors.lastname: Yang
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Liu
authors.forename: Jian-Min
authors.initials: JM
authors.lastname: Chen
authors.forename: Bayasi
authors.initials: B
authors.lastname: Guleng
authors.forename: Jian-Lin
authors.initials: JL
authors.lastname: Ren
mesh_terms: D017209:Apoptosis; D015153:Blotting, Western; D002454:Cell Differentiation; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D015536:Down-Regulation; D004789:Enzyme Activation; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D057809:HEK293 Cells; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D010766:Phosphorylation; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D014162:Transfection; D020741:rho GTP-Binding Proteins / Q000235:genetics / Q000378:metabolism*
chemical_list: C117386:DIRAS3 protein, human; D012333:RNA, Messenger; D020741:rho GTP-Binding Proteins