title: MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells.
abstract: How lncRNA MALAT1 is regulated by miRNAs at posttranscriptional level in pancreatic cancer and their regulative effects on the cancer cells remain largely unknown. By retrieving previous miRNA array data and performing primary qRT-PCR, we observed a significant negative correlation between miR-216a and MALAT1 in pancreatic ductal adenocarcinoma (PDAC) tissues and adjacent normal tissues. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression had similar effects as MALAT1 siRNA on restoring p21 and p27 expression and inhibiting B-MYB, RAF1 and PCNA1 expression in both PANC-1 and BxPC3 cells. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase. MiR-216a overexpression not only significantly induced cell apoptosis, but also reduced cell viability and increased cell apoptosis in response to gemcitabine in the cancer cells. Based on these findings, we infer that miR-216a induces apoptosis both in the presence and absence of gemcitabine in pancreatic cancer cells by silencing MALAT1 expression.
authors.affiliation: Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
authors.forename: Yajing
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Tang
authors.affiliation: Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
authors.forename: Minmin
authors.initials: M
authors.lastname: Shi
authors.affiliation: Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
authors.forename: Chenlei
authors.initials: C
authors.lastname: Wen
authors.affiliation: Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China. Electronic address: baiyongshen@outlook.com.
authors.forename: Baiyong
authors.initials: B
authors.lastname: Shen
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000494:pharmacology; D059565:G2 Phase Cell Cycle Checkpoints / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D055785:Gene Knockdown Techniques; D006801:Humans; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D012323:RNA Processing, Post-Transcriptional; D062085:RNA, Long Noncoding / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D000093542:Gemcitabine
chemical_list: D000970:Antineoplastic Agents; C557041:MALAT1 long non-coding RNA, human; C575482:MIRN216 microRNA, human; D035683:MicroRNAs; D062085:RNA, Long Noncoding; D003841:Deoxycytidine; D000093542:Gemcitabine
keywords: Gemcitabine; MALAT1; MiR-216a; Pancreatic cancer