title: MiR-96 promotes proliferation and chemo- or radioresistance by down-regulating RECK in esophageal cancer.
abstract: The involvement of miR-96 in esophageal cancer (EC) remains unclear. The aim of this study is to explore the functional role of miR-96 and determine whether miR-96 could be a potential therapeutic target for human esophageal cancer. MiR-96 up-regulation was demonstrated in 145 EC samples and RECK down-regulation was validated in EC cell lines. Moreover, ectopic overexpression of miR-96 in TE-1 or ECa-109 contributed to tumor growth in xenograft mouse models. Furthermore, up-regulation of miR-96 could reduce the susceptibilities of EC cells to chemotherapy or radiotherapy. RECK was identified as a target of miR-96 and RECK overexpressing could abrogate the growth of EC cells induced by miR-96. Taken together, miR-96 serves as an oncogene role in EC cells through downregulating RECK.
authors.affiliation: Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006 Jiangsu Province, People's Republic of China.
authors.forename: Haifeng
authors.initials: H
authors.lastname: Xia
authors.affiliation: Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006 Jiangsu Province, People's Republic of China.
authors.forename: Shaomu
authors.initials: S
authors.lastname: Chen
authors.affiliation: Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006 Jiangsu Province, People's Republic of China.
authors.forename: Ke
authors.initials: K
authors.lastname: Chen
authors.affiliation: Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006 Jiangsu Province, People's Republic of China.
authors.forename: Haitao
authors.initials: H
authors.lastname: Huang
authors.affiliation: Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006 Jiangsu Province, People's Republic of China. Electronic address: haitaomasoochow@163.com.
authors.forename: Haitao
authors.initials: H
authors.lastname: Ma
mesh_terms: D000368:Aged; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D045744:Cell Line, Tumor; D015536:Down-Regulation / Q000502:physiology*; D019008:Drug Resistance, Neoplasm / Q000187:drug effects / Q000502:physiology*; D004938:Esophageal Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000532:radiotherapy*; D005260:Female; D058851:GPI-Linked Proteins / Q000378:metabolism*; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D035683:MicroRNAs / Q000096:biosynthesis*; D008875:Middle Aged
chemical_list: D000970:Antineoplastic Agents; D058851:GPI-Linked Proteins; C541492:MIRN96 microRNA, human; D035683:MicroRNAs; C115460:RECK protein, human
keywords: Chemotherapy; EC; MiR-96; RECK; Radiotherapy; Tumor growth