The role of miR-10b-5p in prostate cancer and its exosome-mediated angiogenesis effect

Objective

Prostate cancer (PCa) continues to be a major cause of cancer-related mortality globally, underscoring the critical need for novel therapeutic strategies. This study investigates the oncogenic function of miR-10b-5p in PCa progression and evaluates its potential as both a diagnostic marker and therapeutic target.

Methods

miR-10b-5p was initially identified as a candidate oncogene through bioinformatic analysis of The Cancer Genome Atlas (TCGA) PCa data, followed by validation of its expression levels in clinical PCa specimens via fluorescence in situ hybridization (FISH). Functional assays (proliferation, migration, invasion) were performed to assess the impact of miR-10b-5p on PCa cell behavior. The tumor suppressor ZMYND11 was confirmed as a direct target of miR-10b-5p using dual-luciferase reporter assays. The pro-angiogenic capacity of PCa-derived exosomes harboring miR-10b-5p was evaluated using in vitro endothelial tube formation assays and in vivo mouse models.

Results

miR-10b-5p expression was significantly elevated in PCa tissues and cell lines, and its levels correlated with aggressive tumor features. Mechanistically, miR-10b-5p directly suppressed ZMYND11 expression, thereby promoting PCa cell proliferation, migration, and invasion. Crucially, exosomes derived from miR-10b-5p-expressing PCa cells exhibited potent pro-angiogenic activity, significantly enhancing endothelial tube formation in vitro and stimulating tumor neovascularization in vivo.

Conclusion

This study demonstrates that miR-10b-5p promotes prostate cancer progression by targeting ZMYND11, while its exosomes additionally exhibit pro-angiogenic effects, providing a novel therapeutic target for clinical intervention.