miR-15b promotes epithelial-mesenchymal transition by inhibiting SMURF2 in pancreatic cancer

  • Authors:
    • Wen-Long Zhang
    • Jian-Hua Zhang
    • Xi-Zhao Wu
    • Tao Yan
    • Wei Lv
  • View Affiliations

  • Published online on: July 9, 2015     https://doi.org/10.3892/ijo.2015.3076
  • Pages: 1043-1053
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Abstract

The epithelial-mesenchymal transition (EMT) is a key developmental program that is often activated during cancer invasion and metastasis. We report here that silencing SMURF2 (SMAD specific E3 ubiquitin protein ligase 2) promoted EMT in HPDE6c7 normal pancreas cells and overexpression of SMURF2 inhibited TGF-β-mediated EMT in the cells. Subsequent studies showed that SMURF2 was downregulated in pancreatic cancer tissues and it promoted mesenchymal-epithelial transition (MET) in pancreatic cancer cells as well as its expression negatively associated with gemcitabine-resistance, but it did not alter cell viability, cell cycle and cell senescence. In addition, we demonstrated that miR‑15b degraded SMURF2 and its overexpression promoted EMT in pancreatic cancer, and its expression was associated with metastasis in the disease. Elucidating molecular mechanism of EMT in pancreatic cancer not only will help us to further understand the pathogenesis and progression of the disease, but also offers new targets for effective therapies.
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September 2015
Volume 47 Issue 3

Print ISSN: 1019-6439
Online ISSN:1791-2423

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APA
Zhang, W., Zhang, J., Wu, X., Yan, T., & Lv, W. (2015). miR-15b promotes epithelial-mesenchymal transition by inhibiting SMURF2 in pancreatic cancer. International Journal of Oncology, 47, 1043-1053. https://doi.org/10.3892/ijo.2015.3076
MLA
Zhang, W., Zhang, J., Wu, X., Yan, T., Lv, W."miR-15b promotes epithelial-mesenchymal transition by inhibiting SMURF2 in pancreatic cancer". International Journal of Oncology 47.3 (2015): 1043-1053.
Chicago
Zhang, W., Zhang, J., Wu, X., Yan, T., Lv, W."miR-15b promotes epithelial-mesenchymal transition by inhibiting SMURF2 in pancreatic cancer". International Journal of Oncology 47, no. 3 (2015): 1043-1053. https://doi.org/10.3892/ijo.2015.3076