Methylation of BNIP3 in pancreatic cancer inhibits the induction of mitochondrial-mediated tumor cell apoptosis

• DOI: 10.18632/oncotarget.18736
• Publication Date: 2017-06-28T10:26:27Z
• Authors: Ye Li; Xu Zhang; Jian Yang; Yi Zhang; Dongming Zhu; Lifeng Zhang; Yanbo Zhu; Dechun Li; Jian Zhou
• Keywords: 0301 basic medicine; 03 medical and health sciences; Research Paper; 3. Good health

// Ye Li 1, 2, * , Xu Zhang 3, 4, Jian Yang Yi 1 Dongming Zhu 2 Lifeng Yanbo 5 Dechun and Zhou Department of General Surgery, The First Affiliated Hospital Soochow University, Suzhou 215006, China Pancreatic Disease Research Centre, 3 Science & Technology Town Hospital, 4 to Nanjing Medical Oncology, These authors have contributed equally this work Correspondence to: Zhou, email: [e-mail] Keywords: BNIP3, HIF-1α, apoptosis, methylation, pancreatic cancer Received: April 19, 2017      Accepted: May 31, Published: June 28, 2017 ABSTRACT Bcl-2 interacting protein (BNIP3) is involved in various cellular processes considered a key regulator hypoxia-induced apoptosis. In the present study, expression BNIP3 tissues, correlation with clinicopathological characteristics prognosis regulation cell lines regard induction apoptosis were investigated. was significantly lower tissues compared normal epithelia associated tumor size, clinical stage, lymph node metastasis. correlated positively proapoptotic Bax negatively antiapoptotic Bcl-2, whereas by independent caspase 9 activation. restoration cells vitro caused loss ΔΨm, increase ROS production, induction. opposite effect observed cells, following silencing RNAi. absence related gene methylation that suppressed binding HIF-1α promoter, 5-Aza-2'-deoxycytidine (Aza-dC) treatment restored sensitized BNIP3-induced findings indicated downregulated resulting reduced Silencing hypoxia-responsive element (HRE) site turn inhibited promoter. data suggest reactivation potential target for therapeutic intervention against cancer.