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neo_2026_250619N272

Title: The miR-5681b/Beclin-1 axis regulates tumor autophagy to affect the proliferation and apoptosis of prostate cancer cells
Author: Yanmei Zhang, Jiaojiao Li, Quan Li, Yuan Cao
Abstract: Prostate cancer (PCa) is a leading cause of cancer-related mortality among men. This study aims to investigate the regulatory effect of microRNA (miR)-5681b, a potential upstream miR of Beclin-1, on PCa cell proliferation and apoptosis. Two PCa cell lines (PC3 and LnCaP cells) with relatively low miR-5681b expression were treated with miR-5681b mimic, pcDNA3.1-Beclin-1, or an autophagy activator Rapamycin. A xenograft tumor model was established in nude mice, and the tumor-bearing mice were treated with agomir miR-5681b. The levels of miR-5681b, Beclin-1 mRNA, and apoptosis- and autophagy-associated proteins were evaluated using western blot and RT-qPCR. The binding between Beclin-1 and miR-5681b was testified by dual-luciferase reporter gene assay. Cell biological behaviors, as well as Ki-67-positive cells and apoptosis in mouse tumor tissues, were examined. The results showed that miR-5681b was downregulated in PCa cells and targeted Beclin-1. miR-5681b overexpression in PCa cells significantly suppressed cell proliferation and B-cell lymphoma 2 (Bcl-2) levels while augmenting cell apoptosis and the levels of Bcl-2-associated X (Bax) and cleaved caspase-3. Importantly, miR-5681b inhibited PCa cell proliferation and autophagy but promoted PCa cell apoptosis, whereas Beclin-1 upregulation reversed these effects. Activating autophagy also reversed miR-5681b-regulated proliferation and apoptosis of PCa cells. In vivo, miR-5681b overexpression inhibited PCa tumor growth by modulating the Beclin-1-mediated autophagy pathway. Collectively, these findings suggested that miR-5681b was lowly expressed in PCa cells, and miR-5681b overexpression inhibited autophagy by targeting Beclin-1, thereby suppressing the growth of PCa.
Keywords: miR-5681b; Beclin-1; prostate cancer; autophagy; proliferation; apoptosis; autophagy agonists; rapamycin
Year: , Volume: , Issue: Page From: , Page To:
doi:10.4149/neo_2026_250619N272


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