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ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway
OBJECTIVE: Rho GTPase-activating protein 30 (ARHGAP30), a member of the Rho GTPase-activating proteins (Rho GAPs) family, plays an important role in the regulation of cytoskeleton organization and cell adhesion. MATERIALS AND METHODS: mRNA and protein expression was assessed by quantitative real-tim...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6204876/ https://www.ncbi.nlm.nih.gov/pubmed/30425532 http://dx.doi.org/10.2147/OTT.S175255 |
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author | Mao, Xiaoliang Tong, Jichun |
author_facet | Mao, Xiaoliang Tong, Jichun |
author_sort | Mao, Xiaoliang |
collection | PubMed |
description | OBJECTIVE: Rho GTPase-activating protein 30 (ARHGAP30), a member of the Rho GTPase-activating proteins (Rho GAPs) family, plays an important role in the regulation of cytoskeleton organization and cell adhesion. MATERIALS AND METHODS: mRNA and protein expression was assessed by quantitative real-time PCR and Western blotting, respectively. Cell Counting Kit-8 (CCK-8) and Transwell assays were conducted to detect cell proliferation, migration, and invasion. RESULTS: ARHGAP30 expression was downregulated in specimens and cell lines of lung cancer in comparison to non-cancerous specimens and normal bronchial epithelial cell lines, respectively. Moreover, in vitro experiments demonstrated that ARHGAP30 overexpression impeded the proliferative, migratory, and invasive abilities of lung cancer cells. Moreover, bioinformatics analysis with The Cancer Genome Atlas (TCGA) lung cancer dataset showed a negative association between ARHGAP30 expression and the Wnt signaling pathway. Enforced expression of ARHGAP30 decreased the mRNA and protein levels of β-catenin, c-Myc, matrix metalloproteinase-2 (MMP-2) and MMP-9. Besides, the β-catenin inhibitor XAV939 blocked the enhanced cell growth, migration, and invasion caused by ARHGAP30 knockdown. Thus, the Wnt/β-catenin pathway mediated the functions of ARHGAP30 in lung cancer cells. CONCLUSION: ARHGAP30 acts as a tumor suppressor in lung cancer by suppressing Wnt/β-catenin signaling. |
format | Online Article Text |
id | pubmed-6204876 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-62048762018-11-13 ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway Mao, Xiaoliang Tong, Jichun Onco Targets Ther Original Research OBJECTIVE: Rho GTPase-activating protein 30 (ARHGAP30), a member of the Rho GTPase-activating proteins (Rho GAPs) family, plays an important role in the regulation of cytoskeleton organization and cell adhesion. MATERIALS AND METHODS: mRNA and protein expression was assessed by quantitative real-time PCR and Western blotting, respectively. Cell Counting Kit-8 (CCK-8) and Transwell assays were conducted to detect cell proliferation, migration, and invasion. RESULTS: ARHGAP30 expression was downregulated in specimens and cell lines of lung cancer in comparison to non-cancerous specimens and normal bronchial epithelial cell lines, respectively. Moreover, in vitro experiments demonstrated that ARHGAP30 overexpression impeded the proliferative, migratory, and invasive abilities of lung cancer cells. Moreover, bioinformatics analysis with The Cancer Genome Atlas (TCGA) lung cancer dataset showed a negative association between ARHGAP30 expression and the Wnt signaling pathway. Enforced expression of ARHGAP30 decreased the mRNA and protein levels of β-catenin, c-Myc, matrix metalloproteinase-2 (MMP-2) and MMP-9. Besides, the β-catenin inhibitor XAV939 blocked the enhanced cell growth, migration, and invasion caused by ARHGAP30 knockdown. Thus, the Wnt/β-catenin pathway mediated the functions of ARHGAP30 in lung cancer cells. CONCLUSION: ARHGAP30 acts as a tumor suppressor in lung cancer by suppressing Wnt/β-catenin signaling. Dove Medical Press 2018-10-24 /pmc/articles/PMC6204876/ /pubmed/30425532 http://dx.doi.org/10.2147/OTT.S175255 Text en © 2018 Mao and Tong. 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 Mao, Xiaoliang Tong, Jichun ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway |
title | ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway |
title_full | ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway |
title_fullStr | ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway |
title_full_unstemmed | ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway |
title_short | ARHGAP30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the Wnt/β-catenin signaling pathway |
title_sort | arhgap30 suppressed lung cancer cell proliferation, migration, and invasion through inhibition of the wnt/β-catenin signaling pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6204876/ https://www.ncbi.nlm.nih.gov/pubmed/30425532 http://dx.doi.org/10.2147/OTT.S175255 |
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