Research Paper Volume 16, Issue 2 pp 1938—1951
Long noncoding RNA MEG3 regulates cell proliferation and apoptosis by disrupting microRNA-9-5p-mediated inhibition of NDRG1 in prostate cancer
- 1 Department of Urology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China
- 2 Tianjin Institute of Urology, Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin 300211, China
- 3 Department of Medical Genetics and Cell Biology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China
Received: September 26, 2023 Accepted: December 15, 2023 Published: January 24, 2024
https://doi.org/10.18632/aging.205472How to Cite
Copyright: © 2024 Lian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: Long noncoding RNA MEG3 has been described to be involved in the regulation of gene expression and cancer progression. However, the role of lncMEG3 in prostate cancer (PCa) remains largely uncharted.
Methods: Differential expression of lncMEG3 was identified in PCa tissues using RNA-sequencing analysis. qRT-PCR was performed to examine the level of lncMEG3. Additionally, cellular fractionation and fluorescent in situ hybridization techniques were employed to determine the localization. Subsequently, functional assays were conducted to evaluate the impact of lncMEG3 and miR-9-5p on PCa proliferation and apoptosis in vitro and in vivo. The interaction between lncMEG3 and miR-9-5p was confirmed using RNA immunoprecipitation. Moreover, luciferase reporter assays were also utilized to investigate the relationship between miR-9-5p and NDRG1.
Results: We observed downregulation of lncMEG3 in PCa cells and tissues. Patients with lower levels of lncMEG3 had a higher likelihood of experiencing biochemical recurrence. Overexpression of lncMEG3 resulted in the inhibition of PCa cell proliferation and the promotion of apoptosis. Moreover, lncMEG3 is competitively bound to miR-9-5p, preventing its inhibitory effect on the target gene NDRG1. This ultimately led to the inhibition of PCa cell proliferation and the promotion of apoptosis. Furthermore, increasing lncMEG3 levels also demonstrated inhibitory effects on PCa proliferation and promotion of apoptosis in vivo.
Conclusions: Our findings uncover a crucial role for lncMEG3 in inhibiting PCa proliferation and promoting apoptosis through disruption of miR-9-5p-mediated inhibition of NDRG1.