MiR-96 promotes proliferation and chemo- or radioresistance by down-regulating RECK in esophageal cancer

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.