Open Access

Activation of platelet protease-activated receptor-1 induces epithelial-mesenchymal transition and chemotaxis of colon cancer cell line SW620

Corrigendum in: /or/35/2/1222

  • Authors:
    • Yitao Jia
    • Suqiao Zhang
    • Lingling Miao
    • Jingbao Wang
    • Zujian Jin
    • Bin Gu
    • Zhihui Duan
    • Zhaolong Zhao
    • Shunmao Ma
    • Wenjin Zhang
    • Zhongxin Li
  • View Affiliations

  • Published online on: April 3, 2015     https://doi.org/10.3892/or.2015.3897
  • Pages: 2681-2688
  • Copyright: © Jia et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

The aim of the present study was to examine the role of protease-activated receptor-1 (PAR1)-stimulated platelet activation in the epithelial-mesenchymal transition (EMT) and migration of colon cancer cells, and to identify the underlying mechanisms. TFLLR-NH2, a PAR1 agonist, was used to activate platelets and the platelet supernatants were used to treat the SW620 colon cancer cell line. Expression of E-cadherin and vimentin on SW620 cells was detected by immunofluorescence and western blotting, and the level of the transforming growth factor β1 (TGF-β1) was measured using ELISA following the activation of platelets by TFLLR-NH2. miR-200b expression was detected using quantitative PCR in SW620 cells. In order to investigate the chemotactic ability of the SW620 cells, the expression of CXC chemokine receptor type 4 (CXCR4) was measured by flow cytometry. Transwell migration assays were performed following exposure of the cells to the supernatant of PAR1-activated platelets. SW620 cells cultured in the supernatant of TFLLR-NH2-activated platelets upregulated E-cadherin expression and downregulated the vimentin expression. In the in vitro platelet culture system, a TFLLR-NH2 dose-dependent increase of secreted TGF-β1 was detected in the supernatant. The activation of PAR1 on the platelets led to the inhibition of miR-200b expression in the SW620 cells that were cultured in platelet-conditioned media. The number of SW620 cells that penetrated through the Transwell membrane increased with the dose of TFLLR-NH2 used to treat the platelets. The percentage of CXCR4-positive SW620 cells was significantly higher when they were exposed to the supernatant of platelets cultured for 24 h with PAR1 agonist than when cultured in non-conditioned media (40.89±6.74 vs. 3.47±1.40%, P<0.01). Platelet activation with a PAR1 agonist triggered TGF-β secretion, which induced EMT of SW620 human colon cancer cells via the downregulation of miR-200b expression, and activated platelets had a chemotactic effect on colon cancer cells mediated by the upregulation of CXCR4 on the cell surface.
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June-2015
Volume 33 Issue 6

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Jia Y, Zhang S, Miao L, Wang J, Jin Z, Gu B, Duan Z, Zhao Z, Ma S, Zhang W, Zhang W, et al: Activation of platelet protease-activated receptor-1 induces epithelial-mesenchymal transition and chemotaxis of colon cancer cell line SW620 Corrigendum in /or/35/2/1222. Oncol Rep 33: 2681-2688, 2015.
APA
Jia, Y., Zhang, S., Miao, L., Wang, J., Jin, Z., Gu, B. ... Li, Z. (2015). Activation of platelet protease-activated receptor-1 induces epithelial-mesenchymal transition and chemotaxis of colon cancer cell line SW620 Corrigendum in /or/35/2/1222. Oncology Reports, 33, 2681-2688. https://doi.org/10.3892/or.2015.3897
MLA
Jia, Y., Zhang, S., Miao, L., Wang, J., Jin, Z., Gu, B., Duan, Z., Zhao, Z., Ma, S., Zhang, W., Li, Z."Activation of platelet protease-activated receptor-1 induces epithelial-mesenchymal transition and chemotaxis of colon cancer cell line SW620 Corrigendum in /or/35/2/1222". Oncology Reports 33.6 (2015): 2681-2688.
Chicago
Jia, Y., Zhang, S., Miao, L., Wang, J., Jin, Z., Gu, B., Duan, Z., Zhao, Z., Ma, S., Zhang, W., Li, Z."Activation of platelet protease-activated receptor-1 induces epithelial-mesenchymal transition and chemotaxis of colon cancer cell line SW620 Corrigendum in /or/35/2/1222". Oncology Reports 33, no. 6 (2015): 2681-2688. https://doi.org/10.3892/or.2015.3897