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TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway

BACKGROUND: Colorectal cancer (CRC) is one of the most lethal malignancies. Tripartite Motif Containing 14 (TRIM14) is a member of TRIM family proteins, which are involved in the pathogenesis of various cancers. This study aimed to investigate TRIM14 expression in CRC tissues, and its effects on the...

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Autores principales: Jin, Zhonghai, Li, Hongguang, Hong, Xiaofei, Ying, Guangrong, Lu, Xiaofeng, Zhuang, Lilei, Wu, Shenbao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288942/
https://www.ncbi.nlm.nih.gov/pubmed/30555277
http://dx.doi.org/10.1186/s12935-018-0701-1
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author Jin, Zhonghai
Li, Hongguang
Hong, Xiaofei
Ying, Guangrong
Lu, Xiaofeng
Zhuang, Lilei
Wu, Shenbao
author_facet Jin, Zhonghai
Li, Hongguang
Hong, Xiaofei
Ying, Guangrong
Lu, Xiaofeng
Zhuang, Lilei
Wu, Shenbao
author_sort Jin, Zhonghai
collection PubMed
description BACKGROUND: Colorectal cancer (CRC) is one of the most lethal malignancies. Tripartite Motif Containing 14 (TRIM14) is a member of TRIM family proteins, which are involved in the pathogenesis of various cancers. This study aimed to investigate TRIM14 expression in CRC tissues, and its effects on the migration and invasion of CRC cell lines. METHODS: TRIM14 mRNA expression was detected by real-time PCR analysis. Cell migration and invasion were measured by Transwell assays. Protein expression was assessed by western blot analysis. RESULTS: The expression of TRIM14 was significantly higher in CRC tissues than in matched non-cancerous tissues. TRIM14 knockdown by specific short hairpin RNA (shRNA) attenuated CRC cell migration and invasion, whereas TRIM14 overexpression caused reverse effect. Moreover, TRIM14 positively regulated the protein levels of sphingosine kinase 1 (SPHK1) and phosphorylated STAT3 (p-STAT3), as well as the mRNA and protein expression of matrix metalloproteinase 2, MMP9 and vascular endothelial growth factor, which are transcriptional targets of the STAT3 signaling pathway. Importantly, the blockage of the SPHK1/STAT3 signaling pathway by SKI-II or AG490 could reverse the TRIM14-promoted CRC cell migration and invasion. CONCLUSIONS: Our results reveal a critical role for TRIM14 in promoting migration and invasion of CRC cells, and suggest TRIM14 may serve as a potential molecular target to prevent CRC metastasis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-018-0701-1) contains supplementary material, which is available to authorized users.
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spelling pubmed-62889422018-12-14 TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway Jin, Zhonghai Li, Hongguang Hong, Xiaofei Ying, Guangrong Lu, Xiaofeng Zhuang, Lilei Wu, Shenbao Cancer Cell Int Primary Research BACKGROUND: Colorectal cancer (CRC) is one of the most lethal malignancies. Tripartite Motif Containing 14 (TRIM14) is a member of TRIM family proteins, which are involved in the pathogenesis of various cancers. This study aimed to investigate TRIM14 expression in CRC tissues, and its effects on the migration and invasion of CRC cell lines. METHODS: TRIM14 mRNA expression was detected by real-time PCR analysis. Cell migration and invasion were measured by Transwell assays. Protein expression was assessed by western blot analysis. RESULTS: The expression of TRIM14 was significantly higher in CRC tissues than in matched non-cancerous tissues. TRIM14 knockdown by specific short hairpin RNA (shRNA) attenuated CRC cell migration and invasion, whereas TRIM14 overexpression caused reverse effect. Moreover, TRIM14 positively regulated the protein levels of sphingosine kinase 1 (SPHK1) and phosphorylated STAT3 (p-STAT3), as well as the mRNA and protein expression of matrix metalloproteinase 2, MMP9 and vascular endothelial growth factor, which are transcriptional targets of the STAT3 signaling pathway. Importantly, the blockage of the SPHK1/STAT3 signaling pathway by SKI-II or AG490 could reverse the TRIM14-promoted CRC cell migration and invasion. CONCLUSIONS: Our results reveal a critical role for TRIM14 in promoting migration and invasion of CRC cells, and suggest TRIM14 may serve as a potential molecular target to prevent CRC metastasis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-018-0701-1) contains supplementary material, which is available to authorized users. BioMed Central 2018-12-11 /pmc/articles/PMC6288942/ /pubmed/30555277 http://dx.doi.org/10.1186/s12935-018-0701-1 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Primary Research
Jin, Zhonghai
Li, Hongguang
Hong, Xiaofei
Ying, Guangrong
Lu, Xiaofeng
Zhuang, Lilei
Wu, Shenbao
TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway
title TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway
title_full TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway
title_fullStr TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway
title_full_unstemmed TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway
title_short TRIM14 promotes colorectal cancer cell migration and invasion through the SPHK1/STAT3 pathway
title_sort trim14 promotes colorectal cancer cell migration and invasion through the sphk1/stat3 pathway
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288942/
https://www.ncbi.nlm.nih.gov/pubmed/30555277
http://dx.doi.org/10.1186/s12935-018-0701-1
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