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The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α

Backgrounds: A number of genetic and biological phenomena imply that tumorigenesis of clear cell renal cell carcinoma (ccRCC) is highly correlated with hypoxia-induced factor-1a (HIF-1α). Recently, research focusing on the post-transcriptional regulation of HIF-1α has provided a new perspective for...

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Autores principales: Shi, Fei, Wei, Di, Zhu, Zheng, Yan, Fei, Wang, Fuli, Zhang, Keke, Li, Xi'an, Zheng, Yu, Yuan, Jiarui, Lu, Zifan, Yuan, Jianlin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6995368/
https://www.ncbi.nlm.nih.gov/pubmed/32047543
http://dx.doi.org/10.7150/jca.36083
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author Shi, Fei
Wei, Di
Zhu, Zheng
Yan, Fei
Wang, Fuli
Zhang, Keke
Li, Xi'an
Zheng, Yu
Yuan, Jiarui
Lu, Zifan
Yuan, Jianlin
author_facet Shi, Fei
Wei, Di
Zhu, Zheng
Yan, Fei
Wang, Fuli
Zhang, Keke
Li, Xi'an
Zheng, Yu
Yuan, Jiarui
Lu, Zifan
Yuan, Jianlin
author_sort Shi, Fei
collection PubMed
description Backgrounds: A number of genetic and biological phenomena imply that tumorigenesis of clear cell renal cell carcinoma (ccRCC) is highly correlated with hypoxia-induced factor-1a (HIF-1α). Recently, research focusing on the post-transcriptional regulation of HIF-1α has provided a new perspective for ccRCC therapy. In this study, we observed the expression pattern of the RNA-binding protein QKI, which could regulate HIF expression in ccRCC both in vitro and in vivo. Methods: Tissue microarraywas subjected to immunohistochemistry and tumour cell lines and nude mice were used for in vitro and in vivo assays. QKI overexpression or knockdown was assessed in renal cancer cells. Results: The overexpression of QKI inhibited the proliferation of the 786-0 and caki-1 cells, blocked the cells' entry into the S phase, and promoted apoptosis. In ectopic-implantation nude mice model, QKI depletion significantly increased tumor sizes and initiation rates. Tissue microarrays showed that the expression of QKI genes, and especially QKI-6, was significantly decreased in tumor tissues compared with these in normal kidney tissues. Moreover, decreased QKI expression was closely correlated with high tumor grade, poor differentiation, and poor survival. Conclusions: QKI may be useful as a novel, independent diagnostic and biological marker for ccRCC.
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spelling pubmed-69953682020-02-11 The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α Shi, Fei Wei, Di Zhu, Zheng Yan, Fei Wang, Fuli Zhang, Keke Li, Xi'an Zheng, Yu Yuan, Jiarui Lu, Zifan Yuan, Jianlin J Cancer Research Paper Backgrounds: A number of genetic and biological phenomena imply that tumorigenesis of clear cell renal cell carcinoma (ccRCC) is highly correlated with hypoxia-induced factor-1a (HIF-1α). Recently, research focusing on the post-transcriptional regulation of HIF-1α has provided a new perspective for ccRCC therapy. In this study, we observed the expression pattern of the RNA-binding protein QKI, which could regulate HIF expression in ccRCC both in vitro and in vivo. Methods: Tissue microarraywas subjected to immunohistochemistry and tumour cell lines and nude mice were used for in vitro and in vivo assays. QKI overexpression or knockdown was assessed in renal cancer cells. Results: The overexpression of QKI inhibited the proliferation of the 786-0 and caki-1 cells, blocked the cells' entry into the S phase, and promoted apoptosis. In ectopic-implantation nude mice model, QKI depletion significantly increased tumor sizes and initiation rates. Tissue microarrays showed that the expression of QKI genes, and especially QKI-6, was significantly decreased in tumor tissues compared with these in normal kidney tissues. Moreover, decreased QKI expression was closely correlated with high tumor grade, poor differentiation, and poor survival. Conclusions: QKI may be useful as a novel, independent diagnostic and biological marker for ccRCC. Ivyspring International Publisher 2020-01-01 /pmc/articles/PMC6995368/ /pubmed/32047543 http://dx.doi.org/10.7150/jca.36083 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Shi, Fei
Wei, Di
Zhu, Zheng
Yan, Fei
Wang, Fuli
Zhang, Keke
Li, Xi'an
Zheng, Yu
Yuan, Jiarui
Lu, Zifan
Yuan, Jianlin
The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α
title The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α
title_full The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α
title_fullStr The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α
title_full_unstemmed The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α
title_short The RNA-binding protein QKI suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of HIF-1α
title_sort rna-binding protein qki suppresses tumorigenesis of clear cell renal cell carcinoma by regulating the expression of hif-1α
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6995368/
https://www.ncbi.nlm.nih.gov/pubmed/32047543
http://dx.doi.org/10.7150/jca.36083
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