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α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling

Colon or colorectal cancer is a common type of human cancer, which originates in the intestine crassum or the rectum. In the United States, colorectal cancer has one of the highest rates of cancer-related mortality. Investigating novel chemotherapeutic approaches is significant in the treatment of c...

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Autores principales: Yao, Jialin, Gao, Peng, Xu, Yang, Li, Zhaozhu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4991732/
https://www.ncbi.nlm.nih.gov/pubmed/27432222
http://dx.doi.org/10.3892/mmr.2016.5525
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author Yao, Jialin
Gao, Peng
Xu, Yang
Li, Zhaozhu
author_facet Yao, Jialin
Gao, Peng
Xu, Yang
Li, Zhaozhu
author_sort Yao, Jialin
collection PubMed
description Colon or colorectal cancer is a common type of human cancer, which originates in the intestine crassum or the rectum. In the United States, colorectal cancer has one of the highest rates of cancer-related mortality. Investigating novel chemotherapeutic approaches is significant in the treatment of cancers, such as colorectal cancer. α-tocopherol ether-linked acetic acid (α-TEA) is a potent anticancer agent in multiple types of human cancer. However, its effect remains to be determined in colon cancer. In this study, HCT116 and SW480 human colon cancer cells were used to investigate the anticancer role of α-TEA. It was demonstrated that α-TEA inhibited cell proliferation, migration and invasion in colon cancer cells. Furthermore, it was shown that α-TEA downregulated the activity of RhoA and phosphorylated Rho-associated protein kinase (ROCK) substrate myosin light chain (MLC) using a pull-down assay and western blotting, respectively, implying that the RhoA/ROCK pathway is involved in α-TEA-mediated cell growth and motility inhibition. In order to confirm this hypothesis a RhoA inhibitor (clostridium botulinum C3 exoenzyme), a ROCK inhibitor (Y27632) and RhoA small interfering (si)RNA were applied to block RhoA/ROCK signaling. This resulted in the attenuation of MLC phosphorylation, and augmentation of α-TEA-mediated growth and motility inhibition in colon cancer cells. In conclusion, these results indicate that α-TEA inhibits growth and motility in colon cancer cells possibly by targeting RhoA/ROCK signaling. Moreover, combined with RhoA or ROCK inhibitors, α-TEA may exhibit a more effective inhibitory role in colon cancer.
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spelling pubmed-49917322016-08-26 α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling Yao, Jialin Gao, Peng Xu, Yang Li, Zhaozhu Mol Med Rep Articles Colon or colorectal cancer is a common type of human cancer, which originates in the intestine crassum or the rectum. In the United States, colorectal cancer has one of the highest rates of cancer-related mortality. Investigating novel chemotherapeutic approaches is significant in the treatment of cancers, such as colorectal cancer. α-tocopherol ether-linked acetic acid (α-TEA) is a potent anticancer agent in multiple types of human cancer. However, its effect remains to be determined in colon cancer. In this study, HCT116 and SW480 human colon cancer cells were used to investigate the anticancer role of α-TEA. It was demonstrated that α-TEA inhibited cell proliferation, migration and invasion in colon cancer cells. Furthermore, it was shown that α-TEA downregulated the activity of RhoA and phosphorylated Rho-associated protein kinase (ROCK) substrate myosin light chain (MLC) using a pull-down assay and western blotting, respectively, implying that the RhoA/ROCK pathway is involved in α-TEA-mediated cell growth and motility inhibition. In order to confirm this hypothesis a RhoA inhibitor (clostridium botulinum C3 exoenzyme), a ROCK inhibitor (Y27632) and RhoA small interfering (si)RNA were applied to block RhoA/ROCK signaling. This resulted in the attenuation of MLC phosphorylation, and augmentation of α-TEA-mediated growth and motility inhibition in colon cancer cells. In conclusion, these results indicate that α-TEA inhibits growth and motility in colon cancer cells possibly by targeting RhoA/ROCK signaling. Moreover, combined with RhoA or ROCK inhibitors, α-TEA may exhibit a more effective inhibitory role in colon cancer. D.A. Spandidos 2016-09 2016-07-18 /pmc/articles/PMC4991732/ /pubmed/27432222 http://dx.doi.org/10.3892/mmr.2016.5525 Text en Copyright: © Yao 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
Yao, Jialin
Gao, Peng
Xu, Yang
Li, Zhaozhu
α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling
title α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling
title_full α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling
title_fullStr α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling
title_full_unstemmed α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling
title_short α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling
title_sort α-tea inhibits the growth and motility of human colon cancer cells via targeting rhoa/rock signaling
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4991732/
https://www.ncbi.nlm.nih.gov/pubmed/27432222
http://dx.doi.org/10.3892/mmr.2016.5525
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