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PAR4 overexpression promotes colorectal cancer cell proliferation and migration

  • Authors:
    • Hongshan Zhang
    • Ping Jiang
    • Chuanrao Zhang
    • Siman Lee
    • Wei Wang
    • Hao Zou
  • View Affiliations / Copyright

    Affiliations: Department of Cardiac Function, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China, Department of Pathology and Pathophysiology, Kunming Medical University, Kunming, Yunnan 650500, P.R. China, Department of Functional Experimental Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China, Department of Biochemistry, Kunming Medical University, Kunming, Yunnan 650500, P.R. China, Department of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5745-5752
    |
    Published online on: September 5, 2018
       https://doi.org/10.3892/ol.2018.9407
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Abstract

Protease‑activated receptor 4 (PAR4), a member of the G‑protein‑coupled receptor family, was previously identified to be involved in the progression of cancer. Previous study revealed that the expression of PAR4 was increased in colorectal cancer tissues compared with the associated normal tissues, particularly in positive lymph node and poorly differentiated types of cancer. We hypothesized that PAR4 serves a function in the progression of colorectal cancer. In the present study, overexpression of PAR4 in colorectal cancer LoVo cells promoted proliferation, anchorage‑independent growth and migration. In vivo, PAR4 increased LoVo cell tumorgenicity. In contrast, knockdown of PAR4 in HT‑29 cells decreased proliferation, anchorage‑independent growth and migration. Mechanistic studies revealed that PAR4 increased the phosphorylation of extracellular‑signal‑regulated kinase 1/2 in colorectal cancer cells, which is the potential molecular mechanism that promotes cellular proliferation and migration. Taken together, the results of the present study indicated that overexpression of PAR4 promoted colorectal cancer cell proliferation, survival and metastasis, indicating that PAR4 is a promising therapeutic target for preventing colon cancer progression.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang H, Jiang P, Zhang C, Lee S, Wang W and Zou H: PAR4 overexpression promotes colorectal cancer cell proliferation and migration. Oncol Lett 16: 5745-5752, 2018.
APA
Zhang, H., Jiang, P., Zhang, C., Lee, S., Wang, W., & Zou, H. (2018). PAR4 overexpression promotes colorectal cancer cell proliferation and migration. Oncology Letters, 16, 5745-5752. https://doi.org/10.3892/ol.2018.9407
MLA
Zhang, H., Jiang, P., Zhang, C., Lee, S., Wang, W., Zou, H."PAR4 overexpression promotes colorectal cancer cell proliferation and migration". Oncology Letters 16.5 (2018): 5745-5752.
Chicago
Zhang, H., Jiang, P., Zhang, C., Lee, S., Wang, W., Zou, H."PAR4 overexpression promotes colorectal cancer cell proliferation and migration". Oncology Letters 16, no. 5 (2018): 5745-5752. https://doi.org/10.3892/ol.2018.9407
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang H, Jiang P, Zhang C, Lee S, Wang W and Zou H: PAR4 overexpression promotes colorectal cancer cell proliferation and migration. Oncol Lett 16: 5745-5752, 2018.
APA
Zhang, H., Jiang, P., Zhang, C., Lee, S., Wang, W., & Zou, H. (2018). PAR4 overexpression promotes colorectal cancer cell proliferation and migration. Oncology Letters, 16, 5745-5752. https://doi.org/10.3892/ol.2018.9407
MLA
Zhang, H., Jiang, P., Zhang, C., Lee, S., Wang, W., Zou, H."PAR4 overexpression promotes colorectal cancer cell proliferation and migration". Oncology Letters 16.5 (2018): 5745-5752.
Chicago
Zhang, H., Jiang, P., Zhang, C., Lee, S., Wang, W., Zou, H."PAR4 overexpression promotes colorectal cancer cell proliferation and migration". Oncology Letters 16, no. 5 (2018): 5745-5752. https://doi.org/10.3892/ol.2018.9407
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