miR-143-3p integrates contractility and growth in benign prostate stromal cells.

BACKGROUND

Prostate smooth muscle contraction and stromal growth are key determinants of voiding symptoms in benign prostatic hyperplasia (BPH), but their regulation by microRNAs is unknown. Here, we assessed the functional role of miR-143-3p in contractility and growth-related functions in human prostate stromal cells.

METHODS

Stromal (WPMY-1) and epithelial (BPH-1) cells were transfected with miR-143-3p mimic or inhibitor and analyzed using functional assays for contraction, proliferation, apoptosis, and viability.

RESULTS

In WPMY-1 cells, miR-143-3p levels were strongly increased by mimic and markedly reduced by inhibitor transfection. In collagen matrix assays, contractions were enhanced by the mimic and reduced by the inhibitor. Similarly, agonist-induced contractions were attenuated by the inhibitor and slightly increased or enhanced by the mimic. These effects were accompanied by reduced calponin expression and reduced actin filaments following inhibitor transfection. The inhibitor further decreased proliferation and viability, reduced colony formation, and increased apoptosis, while the mimic exerted opposite or minor effects. In contrast, despite effective modulation of miR-143-3p expression, BPH-1 epithelial cells showed negligible functional responses.

CONCLUSIONS

miR-143-3p promotes contractility and growth while suppressing apoptosis in prostate stromal cells, indicating a coordinated regulation of BPH-relevant functions. Targeting miR-143-3p may represent a strategy to modulate stromal cell function in BPH and associated voiding symptoms.