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环状 RNA CSNK1G3 通过 TIMP3 介导的上皮间质转化促进肾细胞癌中 miR-181b 的上调，从而促进生长和转移。

CircCSNK1G3 up-regulates miR-181b to promote growth and metastasis via TIMP3-mediated epithelial to mesenchymal transitions in renal cell carcinoma.

机构信息

Department of Emergency, Renmin Hospital of Wuhan University, Wuhan, China.

Department of Pharmacy, Renmin Hospital of Wuhan University, Wuhan, China.

出版信息

J Cell Mol Med. 2022 Mar;26(6):1729-1741. doi: 10.1111/jcmm.15911. Epub 2021 Feb 9.

DOI:10.1111/jcmm.15911
PMID:33560588
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8918408/
Abstract

Renal cell carcinoma (RCC) is the most common form of kidney cancer, with a high recurrence rate and metastasis capacity. Circular RNAs (circRNAs) have been suggested to act as the critical regulator in several diseases. This study is designed to investigate the role of circCSNK1G3 on RCC progression. We observed a highly expression of circCSNK1G3 in RCC tissues compared with normal tissues. The aberrantly circCSNK1G3 promoted the tumour growth and metastasis in RCC. In the subsequent mechanism investigation, we discovered that the tumour-promoting effects of circCSNK1G3 were, at least partly, achieved by up-regulating miR-181b. Increased miR-181b inhibits several tumour suppressor gene, including CYLD, LATS2, NDRG2 and TIMP3. Furthermore, the decreased TIMP3 leads to the enhanced epithelial to mesenchymal transition (EMT) process, thus promoting the cancer metastasis. In conclusion, we identified the oncogenic role of circCSNK1G3 in RCC progression and demonstrated the regulatory role of circCSNK1G3 induced miR-181b expression, which leads to TIMP3-mediated EMT process, thus resulting in tumour growth and metastasis in RCC. This study reveals the promise of circCSNK1G3 to be developed as a potential diagnostic and prognostic biomarker in the clinic. And the roles of circCSNK1G3 in cancer research deserve further investigation.

摘要

肾细胞癌（RCC）是最常见的肾癌类型，具有较高的复发率和转移能力。环状 RNA（circRNA）被认为在多种疾病中起关键调节作用。本研究旨在探讨 circCSNK1G3 在 RCC 进展中的作用。我们观察到 RCC 组织中 circCSNK1G3 的表达水平明显高于正常组织。异常表达的 circCSNK1G3 促进了 RCC 肿瘤的生长和转移。在随后的机制研究中，我们发现 circCSNK1G3 的促瘤作用至少部分是通过上调 miR-181b 实现的。增加的 miR-181b 抑制了几个肿瘤抑制基因，包括 CYLD、LATS2、NDRG2 和 TIMP3。此外，TIMP3 的减少导致上皮间质转化（EMT）过程增强，从而促进癌症转移。总之，我们确定了 circCSNK1G3 在 RCC 进展中的致癌作用，并证明了 circCSNK1G3 诱导的 miR-181b 表达的调节作用，导致 TIMP3 介导的 EMT 过程，从而导致 RCC 中的肿瘤生长和转移。这项研究表明 circCSNK1G3 有希望成为临床诊断和预后的潜在生物标志物。并且 circCSNK1G3 在癌症研究中的作用值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5563/8918408/12c7908b9de6/JCMM-26-1729-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5563/8918408/8cb4c75ddd08/JCMM-26-1729-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5563/8918408/6c5c156af22f/JCMM-26-1729-g005.jpg
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