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WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression

BACKGROUND: WISP-1 is a member of the CCN family of growth factors and has been reported to play an important role in tumorigenesis by triggering downstream events via integrin signaling. However, little is known about the role of WISP-1 in proliferation of salivary gland carcinoma (SGC) cells. METH...

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Autores principales: Li, Fu-Jun, Wang, Xin-Juan, Zhou, Xiao-Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5085305/
https://www.ncbi.nlm.nih.gov/pubmed/27799801
http://dx.doi.org/10.2147/OTT.S107166
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author Li, Fu-Jun
Wang, Xin-Juan
Zhou, Xiao-Li
author_facet Li, Fu-Jun
Wang, Xin-Juan
Zhou, Xiao-Li
author_sort Li, Fu-Jun
collection PubMed
description BACKGROUND: WISP-1 is a member of the CCN family of growth factors and has been reported to play an important role in tumorigenesis by triggering downstream events via integrin signaling. However, little is known about the role of WISP-1 in proliferation of salivary gland carcinoma (SGC) cells. METHODS: In this study, we investigated the WISP-1 expression in SGC tissues via immunohistochemical staining, Western blotting assay, and real-time quantitative polymerase chain reaction method, and then evaluated the regulatory role of WISP-1 in the growth of SGC A-253 cells. In addition, the role of MMP-2 in the WISP-1-mediated growth regulation was also investigated. RESULTS: It was demonstrated that the WISP-1 expression was upregulated at both mRNA and protein levels in 15 of 21 SGC tumor tissues, compared to the non-tumor tissues (five of 21), associated with the lymph node dissection and bone invasion. The in vitro CCK-8 assay and colony-forming assay demonstrated that the exogenous WISP-1 treatment or the WISP-1 overexpression promoted the growth of A-253 cells. In addition, we confirmed that the WISP-1 overexpression upregulated the MMP-2 expression in A-253 cells with the gain-of-function and loss-of-function strategies, and that the MMP-2 knockdown attenuated the WISP-1-mediated growth promotion of A-253 cells. CONCLUSION: We found that WISP-1 was overexpressed in the human SGCs, and the WISP-1 overexpression promoted the salivary gland cell proliferation via upregulating MMP-2 expression. Our study recognized the oncogenic role of WISP-1 in human SGCs, which could serve as a potential target for anticancer therapy.
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spelling pubmed-50853052016-10-31 WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression Li, Fu-Jun Wang, Xin-Juan Zhou, Xiao-Li Onco Targets Ther Original Research BACKGROUND: WISP-1 is a member of the CCN family of growth factors and has been reported to play an important role in tumorigenesis by triggering downstream events via integrin signaling. However, little is known about the role of WISP-1 in proliferation of salivary gland carcinoma (SGC) cells. METHODS: In this study, we investigated the WISP-1 expression in SGC tissues via immunohistochemical staining, Western blotting assay, and real-time quantitative polymerase chain reaction method, and then evaluated the regulatory role of WISP-1 in the growth of SGC A-253 cells. In addition, the role of MMP-2 in the WISP-1-mediated growth regulation was also investigated. RESULTS: It was demonstrated that the WISP-1 expression was upregulated at both mRNA and protein levels in 15 of 21 SGC tumor tissues, compared to the non-tumor tissues (five of 21), associated with the lymph node dissection and bone invasion. The in vitro CCK-8 assay and colony-forming assay demonstrated that the exogenous WISP-1 treatment or the WISP-1 overexpression promoted the growth of A-253 cells. In addition, we confirmed that the WISP-1 overexpression upregulated the MMP-2 expression in A-253 cells with the gain-of-function and loss-of-function strategies, and that the MMP-2 knockdown attenuated the WISP-1-mediated growth promotion of A-253 cells. CONCLUSION: We found that WISP-1 was overexpressed in the human SGCs, and the WISP-1 overexpression promoted the salivary gland cell proliferation via upregulating MMP-2 expression. Our study recognized the oncogenic role of WISP-1 in human SGCs, which could serve as a potential target for anticancer therapy. Dove Medical Press 2016-10-21 /pmc/articles/PMC5085305/ /pubmed/27799801 http://dx.doi.org/10.2147/OTT.S107166 Text en © 2016 Li 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
Li, Fu-Jun
Wang, Xin-Juan
Zhou, Xiao-Li
WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression
title WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression
title_full WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression
title_fullStr WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression
title_full_unstemmed WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression
title_short WISP-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating MMP-2 expression
title_sort wisp-1 overexpression upregulates cell proliferation in human salivary gland carcinomas via regulating mmp-2 expression
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5085305/
https://www.ncbi.nlm.nih.gov/pubmed/27799801
http://dx.doi.org/10.2147/OTT.S107166
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