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Article

Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells

  • Authors:
    • Dan Xu
    • Jianxiang Tan
    • Ming Zhou
    • Bimei Jiang
    • Huiqing Xie
    • Xinmin Nie
    • Kun Xia
    • Jianda Zhou
  • View Affiliations / Copyright

    Affiliations: Department of Plastic Surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan 410013, P.R. China, Department of Cancer Research, XiangYa School of Medicine, Changsha, Hunan 410013, P.R. China, Department of Pathophysiology, XiangYa School of Medicine, Changsha, Hunan 410013, P.R. China, Chinese State Key Laboratory of Medical Genetics, Changsha, Hunan 410013, P.R. China
  • Pages: 941-946
    |
    Published online on: August 23, 2012
       https://doi.org/10.3892/ol.2012.878
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Abstract

Cutaneous melanoma is an aggressive form of human skin cancer characterized by high metastatic potential and poor prognosis. Biomarkers of metastatic risk are critically needed to instigate new auxiliary measures in high-risk patients. In clinical specimens of skin melanoma, we previously found that let-7b, microRNA-199a and microRNA-33 were significantly associated with metastatic melanoma, and thus may be the key to melanoma treatment. In this study, we examined the effect of overexpression and inhibition of let-7b and microRNA-199a. Plasmids overexpressing these genes were transfected into B16F10 melanoma cells, and let-7b and microRNA-199a expression were evaluated at the RNA, protein and cellular level. Cyclin D1 expression was significantly higher in cells transfected with let-7b plasmid and let-7b inhibitor compared with control cells (P<0.05). In turn, Met expression in the microRNA-199a plasmid group and microRNA-199a inhibitor group was significantly higher than in the control group (P<0.05). The proliferation rate of B16F10 cells transfected with let-7b or microRNA-199a was lower than that of the control group, particularly until the third day after transfection when the proliferation rate dropped to the lowest value (P<0.05). In addition, the apoptosis rates of the let-7b plasmid group and microRNA-199a plasmid group were significantly higher compared to that of the control group (P<0.05). These results suggest that let-7b and microRNA‑199a may be negative regulators of B16F10 cell proliferation.
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Copy and paste a formatted citation
Spandidos Publications style
Xu D, Tan J, Zhou M, Jiang B, Xie H, Nie X, Xia K and Zhou J: Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells. Oncol Lett 4: 941-946, 2012.
APA
Xu, D., Tan, J., Zhou, M., Jiang, B., Xie, H., Nie, X. ... Zhou, J. (2012). Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells. Oncology Letters, 4, 941-946. https://doi.org/10.3892/ol.2012.878
MLA
Xu, D., Tan, J., Zhou, M., Jiang, B., Xie, H., Nie, X., Xia, K., Zhou, J."Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells". Oncology Letters 4.5 (2012): 941-946.
Chicago
Xu, D., Tan, J., Zhou, M., Jiang, B., Xie, H., Nie, X., Xia, K., Zhou, J."Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells". Oncology Letters 4, no. 5 (2012): 941-946. https://doi.org/10.3892/ol.2012.878
Copy and paste a formatted citation
x
Spandidos Publications style
Xu D, Tan J, Zhou M, Jiang B, Xie H, Nie X, Xia K and Zhou J: Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells. Oncol Lett 4: 941-946, 2012.
APA
Xu, D., Tan, J., Zhou, M., Jiang, B., Xie, H., Nie, X. ... Zhou, J. (2012). Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells. Oncology Letters, 4, 941-946. https://doi.org/10.3892/ol.2012.878
MLA
Xu, D., Tan, J., Zhou, M., Jiang, B., Xie, H., Nie, X., Xia, K., Zhou, J."Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells". Oncology Letters 4.5 (2012): 941-946.
Chicago
Xu, D., Tan, J., Zhou, M., Jiang, B., Xie, H., Nie, X., Xia, K., Zhou, J."Let-7b and microRNA-199a inhibit the proliferation of B16F10 melanoma cells". Oncology Letters 4, no. 5 (2012): 941-946. https://doi.org/10.3892/ol.2012.878
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