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

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 progressio...

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Autores principales: Li, Wen, Song, Yang‐Yi‐Yan, Rao, Ting, Yu, Wei‐Min, Ruan, Yuan, Ning, Jin‐Zhuo, Yao, Xiao‐Bing, Yang, Song‐Yi‐Sha, Cheng, Fan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8918408/
https://www.ncbi.nlm.nih.gov/pubmed/33560588
http://dx.doi.org/10.1111/jcmm.15911
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author Li, Wen
Song, Yang‐Yi‐Yan
Rao, Ting
Yu, Wei‐Min
Ruan, Yuan
Ning, Jin‐Zhuo
Yao, Xiao‐Bing
Yang, Song‐Yi‐Sha
Cheng, Fan
author_facet Li, Wen
Song, Yang‐Yi‐Yan
Rao, Ting
Yu, Wei‐Min
Ruan, Yuan
Ning, Jin‐Zhuo
Yao, Xiao‐Bing
Yang, Song‐Yi‐Sha
Cheng, Fan
author_sort Li, Wen
collection PubMed
description 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.
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spelling pubmed-89184082022-03-18 CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma Li, Wen Song, Yang‐Yi‐Yan Rao, Ting Yu, Wei‐Min Ruan, Yuan Ning, Jin‐Zhuo Yao, Xiao‐Bing Yang, Song‐Yi‐Sha Cheng, Fan J Cell Mol Med Original Articles 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. John Wiley and Sons Inc. 2021-02-09 2022-03 /pmc/articles/PMC8918408/ /pubmed/33560588 http://dx.doi.org/10.1111/jcmm.15911 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Li, Wen
Song, Yang‐Yi‐Yan
Rao, Ting
Yu, Wei‐Min
Ruan, Yuan
Ning, Jin‐Zhuo
Yao, Xiao‐Bing
Yang, Song‐Yi‐Sha
Cheng, Fan
CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
title CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
title_full CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
title_fullStr CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
title_full_unstemmed CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
title_short CircCSNK1G3 up‐regulates miR‐181b to promote growth and metastasis via TIMP3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
title_sort circcsnk1g3 up‐regulates mir‐181b to promote growth and metastasis via timp3‐mediated epithelial to mesenchymal transitions in renal cell carcinoma
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8918408/
https://www.ncbi.nlm.nih.gov/pubmed/33560588
http://dx.doi.org/10.1111/jcmm.15911
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