کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2524254 | 1119552 | 2014 | 8 صفحه PDF | دانلود رایگان |

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.
Journal: Biomedicine & Pharmacotherapy - Volume 68, Issue 8, October 2014, Pages 951–958