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环状 RNA circABCC4 通过作为 miR-1182 的 ceRNA 促进 FOXP4 表达促进前列腺癌进展。

Circular RNA circABCC4 as the ceRNA of miR-1182 facilitates prostate cancer progression by promoting FOXP4 expression.

机构信息

Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, P.R. China.

出版信息

J Cell Mol Med. 2019 Sep;23(9):6112-6119. doi: 10.1111/jcmm.14477. Epub 2019 Jul 3.

DOI:10.1111/jcmm.14477
PMID:31270953
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6714494/
Abstract

In recent years, circular RNAs (circRNAs) have been identified to be essential regulators of various human cancers. However, knowledge of the functions of circRNAs in prostate cancer remains very limited. The correlation between circABCC4 and human cancer is largely unknown. This study aims to investigate the biological functions of circABCC4 in prostate cancer progression and illustrate the underlying mechanism. We found that circABCC4 was remarkably up-regulated in prostate cancer tissues and cell lines and promoted FOXP4 expression by sponging miR-1182 in prostate cancer cells. CircABCC4 knockdown markedly suppressed prostate cancer cell proliferation, cell-cycle progression, migration and invasion in vitro. Furthermore, silencing of the circRNA also delayed tumor growth in vivo. Taken together, our findings indicated that circABCC4 facilitates the malignant behaviour of prostate cancer by promoting FOXP4 expression through sponging of miR-1182. The circABCC4-miR-1182-FOXP4 regulatory loop may be a promising therapeutic target for prostate cancer intervention.

摘要

近年来,环状 RNA(circRNAs)已被确定为多种人类癌症的重要调控因子。然而,circRNAs 在前列腺癌中的功能知之甚少。circABCC4 与人类癌症的相关性在很大程度上尚不清楚。本研究旨在探讨 circABCC4 在前列腺癌进展中的生物学功能,并阐明其潜在机制。我们发现 circABCC4 在前列腺癌组织和细胞系中显著上调,并通过海绵吸附 miR-1182 在前列腺癌细胞中促进 FOXP4 的表达。circABCC4 敲低显著抑制前列腺癌细胞的体外增殖、细胞周期进程、迁移和侵袭。此外,circRNA 的沉默也延迟了体内肿瘤的生长。总之,我们的研究结果表明,circABCC4 通过海绵吸附 miR-1182 促进 FOXP4 表达,促进前列腺癌细胞的恶性行为。circABCC4-miR-1182-FOXP4 调控环可能是前列腺癌干预的有前途的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/bcc69704919d/JCMM-23-6112-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/7b574b177483/JCMM-23-6112-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/6b99945900f5/JCMM-23-6112-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/d0255304e039/JCMM-23-6112-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/14d59ad3bf6f/JCMM-23-6112-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/66731169c0e4/JCMM-23-6112-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/bcc69704919d/JCMM-23-6112-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/7b574b177483/JCMM-23-6112-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/6b99945900f5/JCMM-23-6112-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/d0255304e039/JCMM-23-6112-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/14d59ad3bf6f/JCMM-23-6112-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/66731169c0e4/JCMM-23-6112-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a48/6714494/bcc69704919d/JCMM-23-6112-g006.jpg

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