LncRNA625 modulates prostate cancer cells proliferation and apoptosis through regulating the Wnt/β-catenin pathway by targeting miR-432

J.-B. Li, F. Liu, B.-P. Zhang, W.-K. Bai, W. Cheng, Y.-H. Zhang, L.-J. Yu

Department of Ultrasound, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang Province, China. yulijuan2003@126.com

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• Oncology

OBJECTIVE: Prostate cancer (PCa) is the second leading contributor to male malignancy-associated death in developed countries. The study aimed to evaluate the effects of lncRNA625/miR-432 on the prostate cancer cells and the underlying molecular mechanism.

PATIENTS AND METHODS: The cell proliferation was detected using the MTT and colony formation, and cells apoptosis and cell cycle were analyzed with the flow cytometry. Luciferase reporter assay was carried out to detect the correlation between miR-432 and TRIM29 and PYGO2. Besides, reverse transcription-PCR and Western blot were performed to detect the mRNA and protein levels in prostate tissues and PC3 cells.

RESULTS: lncRNA625 and miR-432 levels were consistently reduced in the PCa tissues compared with the healthy control and lncRNA625 levels significantly affect the miR-432 expression in PC3 cells, indicating that miR-432 is a direct target of lncRNA625. Besides, lncRNA625 overexpression could inhibit the cancer cells growth, arresting cell cycle progression at the G1/S phase, and significantly induce apoptosis of PC3 cells, but reversed by the miR-432 inhibitor. Most importantly, we further found that miR-432 could deactivate Wnt/β-catenin pathway via suppressing TRIM29 and PYGO2 directly.

CONCLUSIONS: lncRNA625 could functionally inhibit PC3 cells proliferation and promote cells apoptosis through regulating the Wnt/β-catenin pathway by targeting miR-432.

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