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TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway

Tripartite motif-containing 59 (TRIM59) belongs to the tripartite motif (TRIM) protein family and is upregulated in various malignancies. However, its expression in colorectal cancer (CRC) is still unknown. In the present study, we examined the expression and biological function of TRIM59 in CRC. We...

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Autores principales: Sun, Ye, Ji, Bing, Feng, Yifei, Zhang, Yue, Ji, Dongjian, Zhu, Chunyan, Wang, Sen, Zhang, Chuan, Zhang, Dongsheng, Sun, Yueming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5492839/
https://www.ncbi.nlm.nih.gov/pubmed/28534983
http://dx.doi.org/10.3892/or.2017.5654
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author Sun, Ye
Ji, Bing
Feng, Yifei
Zhang, Yue
Ji, Dongjian
Zhu, Chunyan
Wang, Sen
Zhang, Chuan
Zhang, Dongsheng
Sun, Yueming
author_facet Sun, Ye
Ji, Bing
Feng, Yifei
Zhang, Yue
Ji, Dongjian
Zhu, Chunyan
Wang, Sen
Zhang, Chuan
Zhang, Dongsheng
Sun, Yueming
author_sort Sun, Ye
collection PubMed
description Tripartite motif-containing 59 (TRIM59) belongs to the tripartite motif (TRIM) protein family and is upregulated in various malignancies. However, its expression in colorectal cancer (CRC) is still unknown. In the present study, we examined the expression and biological function of TRIM59 in CRC. We analyzed CRC tissues and cells by quantitative real-time polymerase chain reaction. Kaplan-Meier survival analysis was used to evaluate the prognostic significance of TRIM59 in CRC patients. Furthermore, we investigated the role of TRIM59 in CRC growth and metastasis. The potential mechanism underlying the regulation of cell metastasis by TRIM59 was determined by western blotting. TRIM59 expression was conspicuously overexpressed in CRC tissues and CRC cell lines compared to that noted in the corresponding normal control cells. Patients with higher TRIM59 expression had poorer prognosis. Furthermore, knockdown of TRIM59 suppressed cell proliferation through the induction of apoptosis and inhibited migration and invasion significantly in vitro. Further investigation revealed that knockdown of TRIM59 effectively reversed the expression of epithelial-mesenchymal transformation-related proteins vimentin, Snail and E-cadherin. Our preliminary results confirm that TRIM59 can be mediated by PI3K/AKT signaling. TRIM59 functions as an oncogene in CRC progression, which could be a novel target for the detection and treatment of CRC.
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spelling pubmed-54928392017-07-06 TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway Sun, Ye Ji, Bing Feng, Yifei Zhang, Yue Ji, Dongjian Zhu, Chunyan Wang, Sen Zhang, Chuan Zhang, Dongsheng Sun, Yueming Oncol Rep Articles Tripartite motif-containing 59 (TRIM59) belongs to the tripartite motif (TRIM) protein family and is upregulated in various malignancies. However, its expression in colorectal cancer (CRC) is still unknown. In the present study, we examined the expression and biological function of TRIM59 in CRC. We analyzed CRC tissues and cells by quantitative real-time polymerase chain reaction. Kaplan-Meier survival analysis was used to evaluate the prognostic significance of TRIM59 in CRC patients. Furthermore, we investigated the role of TRIM59 in CRC growth and metastasis. The potential mechanism underlying the regulation of cell metastasis by TRIM59 was determined by western blotting. TRIM59 expression was conspicuously overexpressed in CRC tissues and CRC cell lines compared to that noted in the corresponding normal control cells. Patients with higher TRIM59 expression had poorer prognosis. Furthermore, knockdown of TRIM59 suppressed cell proliferation through the induction of apoptosis and inhibited migration and invasion significantly in vitro. Further investigation revealed that knockdown of TRIM59 effectively reversed the expression of epithelial-mesenchymal transformation-related proteins vimentin, Snail and E-cadherin. Our preliminary results confirm that TRIM59 can be mediated by PI3K/AKT signaling. TRIM59 functions as an oncogene in CRC progression, which could be a novel target for the detection and treatment of CRC. D.A. Spandidos 2017-07 2017-05-22 /pmc/articles/PMC5492839/ /pubmed/28534983 http://dx.doi.org/10.3892/or.2017.5654 Text en Copyright: © Sun et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Sun, Ye
Ji, Bing
Feng, Yifei
Zhang, Yue
Ji, Dongjian
Zhu, Chunyan
Wang, Sen
Zhang, Chuan
Zhang, Dongsheng
Sun, Yueming
TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway
title TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway
title_full TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway
title_fullStr TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway
title_full_unstemmed TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway
title_short TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway
title_sort trim59 facilitates the proliferation of colorectal cancer and promotes metastasis via the pi3k/akt pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5492839/
https://www.ncbi.nlm.nih.gov/pubmed/28534983
http://dx.doi.org/10.3892/or.2017.5654
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