期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 68, 期 8, 页码 951-958出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2014.10.023
关键词
MiR-96; EC; Chemotherapy; Radiotherapy; RECK; Tumor growth
资金
- National Science and Technology Support Program [BAI02A02 [1]-01]
- project of Ministry of Higher Education
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. (C) 2014 Elsevier Masson SAS. All rights reserved.
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