A novel microRNA-1207-3p/FNDC1/FN1/AR regulatory pathway in prostate cancer.

RNA Dis

Department of Biological Sciences, Hunter College of The City University of New York, New York, NY, 10065, USA; The Graduate Center Departments of Biology and Biochemistry, The City University of New York, New York, NY, 10016, USA; Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, 10065, USA.

Published: February 2017

Prostate cancer (PCa) is the second most common cause of cancer-specific deaths in the U.S. Unfortunately, the underlying molecular mechanisms for its development and progression remain unclear. Studies have established that microRNAs (miRNAs) are dysregulated in PCa. The intron-derived microRNA-1207-3p (miR-1207-3p) is encoded at the non-protein coding gene locus on the 8q24 human chromosomal region, an established PCa susceptibility locus. However, miR-1207-3p in PCa had not previously been investigated. Therefore, we explored if miR-1207-3p plays any regulatory role in PCa. We discovered that miR-1207-3p is significantly underexpressed in PCa cell lines in comparison to normal prostate epithelial cells, and that increased expression of microRNA-1207-3p in PCa cells significantly inhibits proliferation, migration, and induces apoptosis via direct molecular targeting of fibronectin type III domain containing 1 (FNDC1). Our studies also revealed significant overexpression of FNDC1, fibronectin (FN1) and the androgen receptor (AR) in human PCa cell lines as well as tissues, and FNDC1, FN1, and AR positively correlate with aggressive PCa. These findings, recently published in Experimental Cell Research, are the first to describe a novel miR-1207-3p/FNDC1/FN1/AR novel regulatory pathway in PCa.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5328418PMC

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