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Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt

Rap2a, a member of the small GTPase superfamily, belongs to Ras superfamily, and its function in cancer progression is still poorly understood. Our previous study indicated that the ectopic expression of Rap2a enhanced the migration and invasion ability of lung cancer cells. However, its expression...

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Autores principales: Wu, Jin-Xia, Du, Wen-Qi, Wang, Xiu-Cun, Wei, Lu-Lu, Huo, Fu-Chun, Pan, Yao-Jie, Wu, Xiao-Jin, Pei, Dong-Sheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5529368/
https://www.ncbi.nlm.nih.gov/pubmed/28747626
http://dx.doi.org/10.1038/s41598-017-06162-7
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author Wu, Jin-Xia
Du, Wen-Qi
Wang, Xiu-Cun
Wei, Lu-Lu
Huo, Fu-Chun
Pan, Yao-Jie
Wu, Xiao-Jin
Pei, Dong-Sheng
author_facet Wu, Jin-Xia
Du, Wen-Qi
Wang, Xiu-Cun
Wei, Lu-Lu
Huo, Fu-Chun
Pan, Yao-Jie
Wu, Xiao-Jin
Pei, Dong-Sheng
author_sort Wu, Jin-Xia
collection PubMed
description Rap2a, a member of the small GTPase superfamily, belongs to Ras superfamily, and its function in cancer progression is still poorly understood. Our previous study indicated that the ectopic expression of Rap2a enhanced the migration and invasion ability of lung cancer cells. However, its expression and molecular mechanism on renal cell carcinoma (RCC) have not been characterized. This study explored the clinical significance and biological function of Rap2a in human RCC. The clinical relevance of Rap2a in RCC was evaluated by immunohistochemical staining using tissue microarray. Our data showed that Rap2a expression was dramatically increased in RCC tissues compared with normal renal tissues. The ectopic expression of Rap2a enhanced the migration and invasive ability of cancer cells. In contrast, downregulation of Rap2a inhibited cell invasion. Rap2a had no effect on the proliferation of RCC cell lines. Meanwhile, Rap2a can regulate the phosphorylation level of Akt in vitro. In vivo studies also showed that Rap2a positively regulated metastasis of renal cancer cells and the expression of p-Akt. These findings indicate that Rap2a promotes RCC metastasis and may serve as a candidate RCC prognostic marker and a potential therapeutic target.
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spelling pubmed-55293682017-08-02 Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt Wu, Jin-Xia Du, Wen-Qi Wang, Xiu-Cun Wei, Lu-Lu Huo, Fu-Chun Pan, Yao-Jie Wu, Xiao-Jin Pei, Dong-Sheng Sci Rep Article Rap2a, a member of the small GTPase superfamily, belongs to Ras superfamily, and its function in cancer progression is still poorly understood. Our previous study indicated that the ectopic expression of Rap2a enhanced the migration and invasion ability of lung cancer cells. However, its expression and molecular mechanism on renal cell carcinoma (RCC) have not been characterized. This study explored the clinical significance and biological function of Rap2a in human RCC. The clinical relevance of Rap2a in RCC was evaluated by immunohistochemical staining using tissue microarray. Our data showed that Rap2a expression was dramatically increased in RCC tissues compared with normal renal tissues. The ectopic expression of Rap2a enhanced the migration and invasive ability of cancer cells. In contrast, downregulation of Rap2a inhibited cell invasion. Rap2a had no effect on the proliferation of RCC cell lines. Meanwhile, Rap2a can regulate the phosphorylation level of Akt in vitro. In vivo studies also showed that Rap2a positively regulated metastasis of renal cancer cells and the expression of p-Akt. These findings indicate that Rap2a promotes RCC metastasis and may serve as a candidate RCC prognostic marker and a potential therapeutic target. Nature Publishing Group UK 2017-07-26 /pmc/articles/PMC5529368/ /pubmed/28747626 http://dx.doi.org/10.1038/s41598-017-06162-7 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Wu, Jin-Xia
Du, Wen-Qi
Wang, Xiu-Cun
Wei, Lu-Lu
Huo, Fu-Chun
Pan, Yao-Jie
Wu, Xiao-Jin
Pei, Dong-Sheng
Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt
title Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt
title_full Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt
title_fullStr Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt
title_full_unstemmed Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt
title_short Rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-Akt
title_sort rap2a serves as a potential prognostic indicator of renal cell carcinoma and promotes its migration and invasion through up-regulating p-akt
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5529368/
https://www.ncbi.nlm.nih.gov/pubmed/28747626
http://dx.doi.org/10.1038/s41598-017-06162-7
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