miR-194 is a negative regulator of GEF-H1 pathway in melanoma

  • Authors:
    • Bingyu Guo
    • Qiang Hui
    • Yu Zhang
    • Peng Chang
    • Kai Tao
  • View Affiliations

  • Published online on: August 12, 2016     https://doi.org/10.3892/or.2016.5020
  • Pages: 2412-2420
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Abstract

The incidence and associated mortality of melanoma continues to increase worldwide. At present, there is no curative therapy for advanced stage of melanoma. It is necessary to find new indicators of prognosis and therapeutic targets. Increasing evidence shows that miRNA can provide potential candidate biomarkers for melanoma and therapeutic targets. GEF-H1, a regulator of RhoA, as oncogenic driver in melanoma, promotes the growth and invasion of melanoma. miR-194 is a tumor-suppressor gene in multiple tumors, such as bladder and non-small cell lung cancer, and clear cell renal cell carcinoma. In the present study, we demonstrated that GEF-H1 serves as target of miR-194. Overexpression of miR-194 downregulates the GEF-H1/RhoA pathway, inhibits melanoma cancer cell proliferation and metastasis. Furthermore, miR-194 expression is negatively associated with tumor-node-metastasis (TNM) stages. Briefly, our findings provided new theoretical basis for melanoma treatment.
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October-2016
Volume 36 Issue 4

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
Guo B, Hui Q, Zhang Y, Chang P and Tao K: miR-194 is a negative regulator of GEF-H1 pathway in melanoma. Oncol Rep 36: 2412-2420, 2016
APA
Guo, B., Hui, Q., Zhang, Y., Chang, P., & Tao, K. (2016). miR-194 is a negative regulator of GEF-H1 pathway in melanoma. Oncology Reports, 36, 2412-2420. https://doi.org/10.3892/or.2016.5020
MLA
Guo, B., Hui, Q., Zhang, Y., Chang, P., Tao, K."miR-194 is a negative regulator of GEF-H1 pathway in melanoma". Oncology Reports 36.4 (2016): 2412-2420.
Chicago
Guo, B., Hui, Q., Zhang, Y., Chang, P., Tao, K."miR-194 is a negative regulator of GEF-H1 pathway in melanoma". Oncology Reports 36, no. 4 (2016): 2412-2420. https://doi.org/10.3892/or.2016.5020