Abstract
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.
Highlights
Prostate cancer is the most common cancer in men and a leading cause of male death from cancer in Western countries
In light of the above, along with studies that established the involvement of Fyn in processes of cellular motility in prostate cancer [10, 11], we demonstrate in the current study that miR-125a-3p down-regulates cellular pathways that account for proliferation and migration of prostate cancer cells, and portray its regulation of key proteins involved in these pathways
In this study we elucidate the role of miR-125a-3p in cellular pathways accounted for motility and migration of prostate cancer cells
Summary
Prostate cancer is the most common cancer in men and a leading cause of male death from cancer in Western countries. Src family kinases (SFKs), members of the Tyrosine Kinasess family, are pleiotropic activators, proto-oncogenes. They play crucial roles in regulation of cell proliferation and cytoskeleton rearrangement [1] by mediating extracellular interactions driven by various molecules, as G protein-coupled receptor (GPCR), c-Met, EGFR, androgen receptor (AR) and integrins [24]. Fyn is upregulated in prostate cancer where it exhibits tumorigenic potential in processes of cellular motility. Its interaction with several signal molecules, including focal adhesion kinase (FAK), Akt and paxillin, that play an essential role in prostate cancer progression, might account for the described cell transformations and possibly lends credence to its role in both cancer progression and metastasis [10-
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