MicroRNA miR-125a-3p modulates molecular pathway of motility and migration in prostate cancer cells

Lihi Ninio-Many1,5, Hadas Grossman1, Mattan Levi1, Sofia Zilber3, Ilan Tsarfaty4, Noam Shomron1, Anna Tuvar3, Dana Chuderland1, Salomon M Stemmer2, Irit Ben-Aharon2*, Ruth Shalgi1*

1 Department of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel-Aviv University, Israel

2 Institute of Oncology, Davidoff Center, Rabin Medical Center, Beilinson Campus, Petah-Tiqva, and Sackler School of Medicine, Tel Aviv University, Israel

3 Department of Pathology, Rabin Medical Center, Beilinson Campus, Petah-Tiqva, Israel

4 Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Israel.

5 This work was performed in partial fulfillment of the requirements for a Ph.D. degree of Lihi Ninio-Many, Sackler Faculty of Medicine, Tel Aviv University, Israel.

* Equal contribution


Irit Ben-Aharon, email:

Keywords: miR-125a-3p, Fyn, migration, prostate cancer, EMT, live imaging, actin cytoskeleton

Received: February 4, 2014 Accepted: April 28, 2014 Published: April 30, 2014


Fyn kinase is implicated in prostate cancer. We illustrate the role of miR-125a-3p in cellular pathways accounted for motility and migration of prostate cancer cells, probably through its regulation on Fyn expression and Fyn-downstream proteins. Prostate cancer PC3 cells were transiently transfected with empty miR-Vec (control) or with miR-125a-3p. Overexpression of miR-125a-3p reduced migration of PC3 cells and increased apoptosis. Live cell confocal imaging indicated that overexpression of miR-125a-3p reduced the cells’ track speed and length and impaired phenotype. Fyn, FAK and paxillin, displayed reduced activity following miR-125a-3p overexpression. Accordingly, actin rearrangement and cells’ protrusion formation were impaired. An inverse correlation between miR-125a-3p and Gleason score was observed in human prostate cancer tissues. Our study demonstrated that miR-125a-3p may regulate migration of prostate cancer cells.

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