Scholarlink

Objective <p>This work aims to delineate the involvement of LINC01082 in bladder cancer (BC) pathogenesis.</p> Methods <p>Significant downregulation of LINC01082 in BC tissues was identified through GEO database analysis (GSE89006). Subsequent validation in GEPIA, TCGA, and clinical cohorts supported these findings. The diagnostic utility was evaluated via ROC curve analysis. Interaction between LINC01082 and miR-1269a, predicted by lncRNASNP, was confirmed by dual luciferase reporter assays. RT-qPCR measured the expression of LINC01082, miR-1269a, and EMT-related genes, while Transwell assays characterized cell migration and invasion.</p> Results <p>LINC01082 was found to be significantly underexpressed in BC tissues and cell lines, with excellent diagnostic efficacy. LINC01082 can specifically bind to miR-1269a. When LINC01082 expression is silenced, BC cells exhibit increased migration and invasion capacities, accompanied by a decline in the epithelial marker E-cadherin and an upregulation of mesenchymal markers, including N-cadherin and vimentin. However, these effects can be effectively reversed by adding the miR-1269a inhibitor.</p> Conclusion <p>LINC01082 can downregulate the expression of miR-1269a, thereby inhibiting the migration, invasion, and EMT of BC cells, ultimately hindering the malignant progression of tumors. This study provides new insights into its anticancer effects and molecular mechanisms.</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

LINC01082 inhibits malignant phenotypes of bladder cancer through sponging miR-1269a

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月28日

查看全文
  • Xiaokang Su,
  • Lina Huang,
  • Yin Yu,
  • Jianbin Zhang

摘要

Objective

This work aims to delineate the involvement of LINC01082 in bladder cancer (BC) pathogenesis.

Methods

Significant downregulation of LINC01082 in BC tissues was identified through GEO database analysis (GSE89006). Subsequent validation in GEPIA, TCGA, and clinical cohorts supported these findings. The diagnostic utility was evaluated via ROC curve analysis. Interaction between LINC01082 and miR-1269a, predicted by lncRNASNP, was confirmed by dual luciferase reporter assays. RT-qPCR measured the expression of LINC01082, miR-1269a, and EMT-related genes, while Transwell assays characterized cell migration and invasion.

Results

LINC01082 was found to be significantly underexpressed in BC tissues and cell lines, with excellent diagnostic efficacy. LINC01082 can specifically bind to miR-1269a. When LINC01082 expression is silenced, BC cells exhibit increased migration and invasion capacities, accompanied by a decline in the epithelial marker E-cadherin and an upregulation of mesenchymal markers, including N-cadherin and vimentin. However, these effects can be effectively reversed by adding the miR-1269a inhibitor.

Conclusion

LINC01082 can downregulate the expression of miR-1269a, thereby inhibiting the migration, invasion, and EMT of BC cells, ultimately hindering the malignant progression of tumors. This study provides new insights into its anticancer effects and molecular mechanisms.