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

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

  • J Cancer Res Clin Oncol. 2025 Mar 4;151(3):98. doi: 10.1007/s00432-025-06153-6.
Yuhui Zhao # 1,  Zhihang Zhang # 2,  Yi Zheng 3,  Huiming Bai 1,  Xiaotong Wu 1,  Yantao Yang 1,  Junfeng Zhang 4,  Chao Yu 5
Affiliations

Affiliations

  • 1 Department of Urology, Longhua Hospital Shanghai University of Traditional Chinese Medicine, No. 725, Wanping South Road, Shanghai, 200032, China.
  • 2 Department of Urology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, 310006, China.
  • 3 Department of Breast Surgery, Zhengzhou Traditional Chinese Medicine Hospital, Zhengzhou, 452400, China.
  • 4 Department of Emergency, Jiaozuo Hospital of Traditional Chinese Medicine, Jiaozuo, 454100, China.
  • 5 Department of Urology, Longhua Hospital Shanghai University of Traditional Chinese Medicine, No. 725, Wanping South Road, Shanghai, 200032, China. chaoyudr1@163.com.
  • # Contributed equally.
PMID: 40035871 DOI: 10.1007/s00432-025-06153-6
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.

Keywords

LINC01128; Prognosis; Progression; Prostate cancer; miR-27b-3p.

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