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

  • Authors:
    • Jialin Yao
    • Peng Gao
    • Yang Xu
    • Zhaozhu Li
  • View Affiliations / Copyright

    Affiliations: Department of Pediatric Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China, Department of Pediatric Surgery, The Harbin Children's Hospital, Harbin, Heilongjiang 150001, P.R. China, Department of Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China
    Copyright: © Yao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2534-2540
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    Published online on: July 18, 2016
       https://doi.org/10.3892/mmr.2016.5525
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Abstract

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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Copy and paste a formatted citation
Spandidos Publications style
Yao J, Gao P, Xu Y and Li Z: α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling. Mol Med Rep 14: 2534-2540, 2016.
APA
Yao, J., Gao, P., Xu, Y., & Li, Z. (2016). α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling. Molecular Medicine Reports, 14, 2534-2540. https://doi.org/10.3892/mmr.2016.5525
MLA
Yao, J., Gao, P., Xu, Y., Li, Z."α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling". Molecular Medicine Reports 14.3 (2016): 2534-2540.
Chicago
Yao, J., Gao, P., Xu, Y., Li, Z."α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling". Molecular Medicine Reports 14, no. 3 (2016): 2534-2540. https://doi.org/10.3892/mmr.2016.5525
Copy and paste a formatted citation
x
Spandidos Publications style
Yao J, Gao P, Xu Y and Li Z: α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling. Mol Med Rep 14: 2534-2540, 2016.
APA
Yao, J., Gao, P., Xu, Y., & Li, Z. (2016). α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling. Molecular Medicine Reports, 14, 2534-2540. https://doi.org/10.3892/mmr.2016.5525
MLA
Yao, J., Gao, P., Xu, Y., Li, Z."α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling". Molecular Medicine Reports 14.3 (2016): 2534-2540.
Chicago
Yao, J., Gao, P., Xu, Y., Li, Z."α-TEA inhibits the growth and motility of human colon cancer cells via targeting RhoA/ROCK signaling". Molecular Medicine Reports 14, no. 3 (2016): 2534-2540. https://doi.org/10.3892/mmr.2016.5525
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