【摘 要】
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PURPOSE:Emerging evidence has indicated that the expression of opioid binding protein/cell adhesion molecule-like (OPCML) gene is frequently altered in a variety of cancers.We previously demonstrated
【机 构】
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Molecular Oncology and Epigenetics Laboratory,the First Affiliated Hospital of Chongqing Medical Uni
【出 处】
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中国病理生理学会第十四届肿瘤专业委员会、第十五届免疫专业委员会联合学术会议
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PURPOSE:Emerging evidence has indicated that the expression of opioid binding protein/cell adhesion molecule-like (OPCML) gene is frequently altered in a variety of cancers.We previously demonstrated that the OPCML gene is a target of epigenetic inactivation in multiple cancers.However,little is known regarding the effects and mechanisms of OPCML in colon cancer.METHODS: Methylation status of OPCML was analyzed by MSP.The impact of OPCML overexpression on the proliferation,cell cycling,apoptosis,colony formation,migration and invasion was characterized.The expression of OPCML and some related factor was examined by PCR and Western blot or immunofluorescence analysis.RESULTS: Methylation of the OPCML promoter was detected in a majority of colon tumor tissues (100% of 50 cases),but significant lower methylation in paired normal colon tissues.The drug-induced release of epigenetic silencing in cells was able to restore OPCML expression and the re-expression led to the suppression of cell growth in vitro via G1 arrest concurrent with apoptosis.Furthermore,the increase in OPCML expression reversed a partial epithelial-to-mesenchymal (EMT)-like transition.Cell migration and invasiveness were also inhibited in response to OPCML upregulation.These actions were mediated through the inactivation of TGFβ-Smad signaling pathways.In addition,OPCML expression was associated with the upstream two nuclear receptor (ERRa and RORa).CONCLUSIONS: our study reveals OPCML as a potential tumor suppressor gene epigenetically silenced in colon cancer.Our study will help to elucidate the anti-invasive mechanisms of OPCML and establish new chemotherapeutic strategies for human colon cancer.
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