ArticleWorld journal of surgical oncology2026
Silencing of ELFN1-AS1 induces prostate cancer cell apoptosis and autophagy by regulating miR-28-5p/BCAM axis.
Article in World journal of surgical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundProstate cancer (PCa) is the most frequently diagnosed non-cutaneous malignancy in men worldwide and constitutes a leading contributor to cancer-related mortality globally. This study aimed to investigate the biological functions and molecular mechanisms of long noncoding RNA ELFN1-AS1 in regulating PCa cell phenotypes.
methodsELFN1-AS1 expression in PCa cells was quantified via RT-qPCR analysis. CCK-8, Transwell, and flow cytometry analysis were carried out to measure PCa cell viability, invasion, and apoptosis. Monodansylcadaverine staining was used to visualize and assess autophagosome formation in PCa cells. Western blot analysis was performed to measure protein levels of apoptotic markers, autophagic markers, and the downstream factor basal cell adhesion molecule (BCAM). The binding relationship among ELFN1-AS1, miR-28-5p, and BCAM were validated by luciferase reporter assay and RNA immunoprecipitation assays.
resultsThe results demonstrated that ELFN1-AS1 and BCAM were highly expressed in PCa cells, while miR-28-5p expression was downregulated compared with normal prostate epithelial cells. Silencing of ELFN1-AS1 effectively reduced optical density values and numbers of invaded cells while concurrently elevating apoptotic proportion. Moreover, ELFN1-AS1 knockdown promoted the formation of autophagosomes and increased LC3II/LC3I ratio. Importantly, ELFN1-AS1 acted as a molecular sponge for miR-28-5p to regulate BCAM expression. Additionally, the inhibitory effects of ELFN1-AS1 depletion on the malignant biological behaviors of PCa cells were notably reversed by BCAM overexpression.
conclusionOur findings indicate that the silencing of ELFN1-AS1 promotes PCa cell apoptosis and autophagy by interacting with miR-28-5p to regulate BCAM expression.
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