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

Biomed Pharmacother. 2014 Oct;68(8):951-8. doi: 10.1016/j.biopha.2014.10.023. Epub 2014 Oct 31.

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.

Keywords: Chemotherapy; EC; MiR-96; RECK; Radiotherapy; Tumor growth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Cell Line, Tumor
  • Down-Regulation / physiology*
  • Drug Resistance, Neoplasm / drug effects
  • Drug Resistance, Neoplasm / physiology*
  • Esophageal Neoplasms / drug therapy
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / radiotherapy*
  • Female
  • GPI-Linked Proteins / metabolism*
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • MicroRNAs / biosynthesis*
  • Middle Aged

Substances

  • Antineoplastic Agents
  • GPI-Linked Proteins
  • MIRN96 microRNA, human
  • MicroRNAs
  • RECK protein, human