Scholarlink

Background <p>Prostate 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.</p> Methods <p>ELFN1-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.</p> Results <p>The 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.</p> Conclusion <p>Our findings indicate that the silencing of ELFN1-AS1 promotes PCa cell apoptosis and autophagy by interacting with miR-28-5p to regulate BCAM expression.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Silencing of ELFN1-AS1 induces prostate cancer cell apoptosis and autophagy by regulating miR-28-5p/BCAM axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月29日

查看全文
  • Shuai Luo,
  • Dingwen Gui,
  • Yankuang Guo,
  • Zuwei Xu,
  • Zheng Fang,
  • Geng Huang,
  • Wenbing Wu

摘要

Background

Prostate 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.

Methods

ELFN1-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.

Results

The 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.

Conclusion

Our findings indicate that the silencing of ELFN1-AS1 promotes PCa cell apoptosis and autophagy by interacting with miR-28-5p to regulate BCAM expression.