RCOR1 is targeted by miR-23b-3p to modulate growth, colony formation, migration, and invasion of prostate cancer cells.

IF 1.1 Q4 ONCOLOGY

International journal of clinical and experimental pathology Pub Date : 2024-02-15 eCollection Date: 2024-01-01

Chenli Liu, Zhong Dong, Maozhang Li, Guangwei Bai, Zhixiang Zhao

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引用次数: 0

Abstract

Objectives: Prostate cancer holds the second-highest incidence rate among all male malignancies, with a noticeable scarcity of effective treatment approaches. The REST Corepressor 1 (RCOR1) protein exhibits elevated expression across various tumors, acting as an oncogene. Nevertheless, its functions and mechanisms in prostate cancer have yet to be documented. While miR-23 demonstrates reduced expression in prostate cancer, the downstream genes it regulates remain unclear.

Methods: RT-qPCR and Western blotting assays were utilized to elucidate the mRNA and protein levels of miR-23b-3p and RCOR1. The luciferase reporter assay was employed to unveil the targeting relationship between miR-23b-3p and RCOR1. Additionally, a CCK-8 assay demonstrated cell growth, while colony formation and Transwell assays were performed to observe clone formation, cell migration, and invasion.

Results: In this study, we observed substantial mRNA and protein levels of RCOR1 in prostate cancer cells such as DU145, PC3, and LNCap. RCOR1 overexpression enhanced the growth, colony formation, migration, and invasion of prostate cancer cells, whereas genetic silencing of RCOR1 suppressed these processes. Bioinformatics analysis identified miR-23b-3p as a potential regulator of RCOR1, and luciferase assays validated RCOR1 as a downstream target of miR-23b-3p. Increasing miR-23b-3p mimics diminished RCOR1's mRNA and protein levels, while raising miR-23b-3p levels boosted RCOR1's expression. Moreover, the stimulatory impact of RCOR1 on prostate cancer cell development could be countered by elevating miR-23b-3p mimics.

Conclusion: In summary, our findings confirm that RCOR1 is indeed under the influence of miR-23, shedding light on the miR-23/RCOR1 pathway's role in prostate cancer development. This offers novel theoretical and experimental support for comprehending the underlying mechanisms of prostate cancer and for targeted therapeutic avenues.

本刊更多论文

RCOR1 是 miR-23b-3p 的靶标，可调节前列腺癌细胞的生长、集落形成、迁移和侵袭。

目标：在所有男性恶性肿瘤中，前列腺癌的发病率位居第二，但有效的治疗方法却明显匮乏。REST Corepressor 1（RCOR1）蛋白在各种肿瘤中都有高表达，是一种致癌基因。然而，它在前列腺癌中的功能和机制尚未得到证实。虽然 miR-23 在前列腺癌中的表达减少，但其调控的下游基因仍不清楚：方法：利用 RT-qPCR 和 Western 印迹分析法阐明 miR-23b-3p 和 RCOR1 的 mRNA 和蛋白水平。荧光素酶报告实验揭示了 miR-23b-3p 和 RCOR1 之间的靶向关系。此外，CCK-8 试验证明了细胞的生长，而集落形成和 Transwell 试验则观察了克隆形成、细胞迁移和侵袭：结果：在这项研究中，我们在 DU145、PC3 和 LNCap 等前列腺癌细胞中观察到了大量的 RCOR1 mRNA 和蛋白水平。RCOR1 的过表达增强了前列腺癌细胞的生长、集落形成、迁移和侵袭，而 RCOR1 的基因沉默则抑制了这些过程。生物信息学分析发现，miR-23b-3p 是 RCOR1 的潜在调节因子，荧光素酶测定验证了 RCOR1 是 miR-23b-3p 的下游靶标。增加 miR-23b-3p 模拟物会降低 RCOR1 的 mRNA 和蛋白水平，而提高 miR-23b-3p 水平则会促进 RCOR1 的表达。此外，RCOR1对前列腺癌细胞发育的刺激作用可以通过提高miR-23b-3p模拟物的水平来抵消：总之，我们的研究结果证实了 RCOR1 确实受到 miR-23 的影响，从而揭示了 miR-23/RCOR1 通路在前列腺癌发展中的作用。这为理解前列腺癌的潜在机制和靶向治疗途径提供了新的理论和实验支持。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International journal of clinical and experimental pathology ONCOLOGY-PATHOLOGY

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The International Journal of Clinical and Experimental Pathology (IJCEP, ISSN 1936-2625) is a peer reviewed, open access online journal. It was founded in 2008 by an international group of academic pathologists and scientists who are devoted to the scientific exploration of human disease and the rapid dissemination of original data. Unlike most other open access online journals, IJCEP will keep all the traditional features of paper print that we are all familiar with, such as continuous volume and issue numbers, as well as continuous page numbers to keep our warm feelings towards an academic journal. Unlike most other open access online journals, IJCEP will keep all the traditional features of paper print that we are all familiar with, such as continuous volume and issue numbers, as well as continuous page numbers to keep our warm feelings towards an academic journal.