FYN promotes breast cancer progression through epithelial-mesenchymal transition

  • Authors:
    • Ye-Gong Xie
    • Yue Yu
    • Li-Kun Hou
    • Xin Wang
    • Bin Zhang
    • Xu-Chen Cao
  • View Affiliations

  • Published online on: June 22, 2016     https://doi.org/10.3892/or.2016.4894
  • Pages: 1000-1006
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Abstract

FYN, one of the members of the Src family of kinases (SFKs), has been reported to be overexpressed in various types of cancers and correlated with cell motility and proliferation. However, the mechanism is still unclear. In the present study, we found that FYN was overexpressed in breast cancer and overexpression of FYN promoted cell proliferation, migration and invasion in the MCF10A cells, whereas depletion of FYN suppressed cell proliferation, migration and invasion in the MDA-MB-231 cells. Moreover, FYN upregulated the expression of mesenchymal markers and epithelial-mesenchymal transition (EMT)-related transcription factors, and downregulated the expression of epithelial markers, suggesting that FYN induces EMT in breast cancer cells. Furthermore, FYN was transcriptionally regulated by FOXO1 and mediated FGF2-induced EMT through both the PI3K/AKT and ERK/MAPK pathways.
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August-2016
Volume 36 Issue 2

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

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Copy and paste a formatted citation
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Spandidos Publications style
Xie Y, Yu Y, Hou L, Wang X, Zhang B and Cao X: FYN promotes breast cancer progression through epithelial-mesenchymal transition. Oncol Rep 36: 1000-1006, 2016
APA
Xie, Y., Yu, Y., Hou, L., Wang, X., Zhang, B., & Cao, X. (2016). FYN promotes breast cancer progression through epithelial-mesenchymal transition. Oncology Reports, 36, 1000-1006. https://doi.org/10.3892/or.2016.4894
MLA
Xie, Y., Yu, Y., Hou, L., Wang, X., Zhang, B., Cao, X."FYN promotes breast cancer progression through epithelial-mesenchymal transition". Oncology Reports 36.2 (2016): 1000-1006.
Chicago
Xie, Y., Yu, Y., Hou, L., Wang, X., Zhang, B., Cao, X."FYN promotes breast cancer progression through epithelial-mesenchymal transition". Oncology Reports 36, no. 2 (2016): 1000-1006. https://doi.org/10.3892/or.2016.4894