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TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway

OBJECTIVE: TMEM119 is a member of transmembrane proteins family, which is abnormally expressed in human cancers and associated with tumorigenesis. In this study, we focused on the expression of TMEM119 and its role in cell invasion and migration in gastric cancer. METHODS: Real-time polymerase chain...

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Autores principales: Zheng, Peifen, Wang, Weifeng, Ji, Muxi, Zhu, Qin, Feng, Yuliang, Zhou, Feng, He, Qiaona
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145364/
https://www.ncbi.nlm.nih.gov/pubmed/30271166
http://dx.doi.org/10.2147/OTT.S164045
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author Zheng, Peifen
Wang, Weifeng
Ji, Muxi
Zhu, Qin
Feng, Yuliang
Zhou, Feng
He, Qiaona
author_facet Zheng, Peifen
Wang, Weifeng
Ji, Muxi
Zhu, Qin
Feng, Yuliang
Zhou, Feng
He, Qiaona
author_sort Zheng, Peifen
collection PubMed
description OBJECTIVE: TMEM119 is a member of transmembrane proteins family, which is abnormally expressed in human cancers and associated with tumorigenesis. In this study, we focused on the expression of TMEM119 and its role in cell invasion and migration in gastric cancer. METHODS: Real-time polymerase chain reaction, Western blotting, and immunohistochemistry were performed to examine the expression of TMEM119 in gastric cancer tissues and cell lines. After transfection with TMEM119 siRNA or recombined TMEM119-expressing vector, the invasion and migration ability of MKN45 and SGC-7901 cells was measured by transwell assay. The expression of TMEM119, p-STAT3, STAT3, VEGF, MMP2, and MMP9 proteins in SGC-7901 and MKN45 cells treated with TMEM119 siRNA, TMEM119-expressing vector, or AG490 was measured by Western blotting. RESULTS: We found that higher TMEM119 expression was found in gastric cancer tissues and cell lines and was associated with lower survival rate. TMEM119 knockdown inhibited SGC-7901 cell invasion and migration, along with the expression of p-STAT3, VEGF, MMP2, and MMP9. TMEM119 overexpression promoted MKN45 cell invasion and migration, along with the expression of p-STAT3, VEGF, MMP2, and MMP9. Additionally, AG490 treatment significantly corrected TMEM119-induced MKN45 cell migration and invasion and expression of p-STAT3, VEGF, MMP9, and MMP2 proteins. CONCLUSION: The results indicated that TMEM119 promotes gastric cancer cell migration and invasion through activation of STAT3 signaling pathway, and TMEM119 may therefore act as a novel therapeutic target for gastric cancer.
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spelling pubmed-61453642018-09-28 TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway Zheng, Peifen Wang, Weifeng Ji, Muxi Zhu, Qin Feng, Yuliang Zhou, Feng He, Qiaona Onco Targets Ther Original Research OBJECTIVE: TMEM119 is a member of transmembrane proteins family, which is abnormally expressed in human cancers and associated with tumorigenesis. In this study, we focused on the expression of TMEM119 and its role in cell invasion and migration in gastric cancer. METHODS: Real-time polymerase chain reaction, Western blotting, and immunohistochemistry were performed to examine the expression of TMEM119 in gastric cancer tissues and cell lines. After transfection with TMEM119 siRNA or recombined TMEM119-expressing vector, the invasion and migration ability of MKN45 and SGC-7901 cells was measured by transwell assay. The expression of TMEM119, p-STAT3, STAT3, VEGF, MMP2, and MMP9 proteins in SGC-7901 and MKN45 cells treated with TMEM119 siRNA, TMEM119-expressing vector, or AG490 was measured by Western blotting. RESULTS: We found that higher TMEM119 expression was found in gastric cancer tissues and cell lines and was associated with lower survival rate. TMEM119 knockdown inhibited SGC-7901 cell invasion and migration, along with the expression of p-STAT3, VEGF, MMP2, and MMP9. TMEM119 overexpression promoted MKN45 cell invasion and migration, along with the expression of p-STAT3, VEGF, MMP2, and MMP9. Additionally, AG490 treatment significantly corrected TMEM119-induced MKN45 cell migration and invasion and expression of p-STAT3, VEGF, MMP9, and MMP2 proteins. CONCLUSION: The results indicated that TMEM119 promotes gastric cancer cell migration and invasion through activation of STAT3 signaling pathway, and TMEM119 may therefore act as a novel therapeutic target for gastric cancer. Dove Medical Press 2018-09-13 /pmc/articles/PMC6145364/ /pubmed/30271166 http://dx.doi.org/10.2147/OTT.S164045 Text en © 2018 Zheng et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Zheng, Peifen
Wang, Weifeng
Ji, Muxi
Zhu, Qin
Feng, Yuliang
Zhou, Feng
He, Qiaona
TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway
title TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway
title_full TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway
title_fullStr TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway
title_full_unstemmed TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway
title_short TMEM119 promotes gastric cancer cell migration and invasion through STAT3 signaling pathway
title_sort tmem119 promotes gastric cancer cell migration and invasion through stat3 signaling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6145364/
https://www.ncbi.nlm.nih.gov/pubmed/30271166
http://dx.doi.org/10.2147/OTT.S164045
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