LncRNA LINC01128 promotes prostate cancer cell proliferation, metastasis, and epithelial-mesenchymal transition by modulating miR-27b-3p.

Abstract

Background: Prostate cancer (PCa) is a prevalent malignancy within the male reproductive system that poses a significant threat to patients' lives. The function of long non-coding RNA LINC01128 in PCa progression remains to be elucidated.

Objective: The objective was to evaluate the significance of LINC01128 in PCa and to elucidate the underlying mechanisms, thereby identifying a potential target for PCa treatment.

Methods: The clinical significance of LINC01128 in PCa was investigated by bioinformatics methods and data analysis. The expression of LINC01128 was quantified using real-time quantitative PCR. The impact of LINC01128 on PCa cell viability and metastasis was evaluated through Cell Counting Kit-8 and Transwell assays. The expression of epithelial-mesenchymal transition markers was analyzed by Western blot analysis. Bioinformatics methods and dual-luciferase reporter assay were employed to explore the mechanisms underlying the role of LINC01128 in PCa progression.

Results: LINC01128 demonstrated significant upregulation in PCa and exhibited a strong correlation with tumor-node-metastasis (TNM) stage, Gleason score, and lymph node metastasis. The upregulation of LINC01128 was found to be linked to a poorer prognosis for PCa. In PCa cells, silencing LINC01128 resulted in the suppression of cell proliferation, migration, and invasion. Furthermore, the knockdown of LINC01128 enhanced the expression of E-cadherin while concurrently repressing the expression of N-cadherin and Vimentin. Mechanistically, the negative regulation of miR-27b-3p by LINC01128 mediated the role of LINC01128 in PCa progression.

Conclusions: In PCa, high expression of LINC01128 may predict patients' unfavorable prognosis. LINC01128 promoted PCa cellular processes by negatively regulating miR-27b-3p.