Universidad de Murcia, Departamento de Biologia Celular e Histiologia
Abstract
Background. Prostate cancer (PC) is the
second leading cause of cancer-related death among men
worldwide. Downregulation of miR-485-3p has been
revealed to participate in the tumorigenesis and
progression of many types of cancer. However, the
clinical and biological role of miR-485-3p in PC remains
largely unknown.
Methods. The expression of miR-485-3p was
analyzed in the published databases and detected in our
clinical samples and cell lines by RT-qPCR assay.
CCK8, transwell invasion and migration, and colony
formation assays were performed to investigate the
biological function of miR-485-3p. Bioinformatical
analysis, RIP, western blotting and luciferase reporter
assays were carried out to explore the downstream
mechanism of miR-485-3p.
Results. The level of miR-485-3p was downregulated in PC tissues, particularly in primary PC
tissues with metastasis relative to normal prostate
tissues. miR-485-3p downregulation was positively
correlated with poor disease-free and overall survival in
patients with PC. Functionally, miR-485-3p overexpression dramatically suppressed the proliferation,
migration and invasion ability of PC cells in vitro.
Mechanistically, miR-485-3p overexpression suppressed
the activity of TGF-β signaling by targeting TGFBR2 to
play tumor-suppressive roles in PC progression.
Conclusion. Our study reports the miR-485-
3p/TGFBR2/ TGF-β signaling axis in tumor
development of PC, suggesting miR-485-3p may be a
potential target to develop therapeutic strategies against
PC