MiR-26b inhibits melanoma cell proliferation and enhances apoptosis by suppressing TRAF5-mediated MAPK activation
| Autor: | Yang Luo, Gui-Lan Yang, Chao-Qin Long, Meng Li, Hua Du |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
MAP Kinase Signaling System Biophysics Down-Regulation Apoptosis Biology Biochemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Annexin Cell Line Tumor medicine Humans Viability assay Fluorescein isothiocyanate Melanoma Molecular Biology Cell Proliferation Mitogen-Activated Protein Kinase Kinases TNF Receptor-Associated Factor 5 Cell growth Cell Biology medicine.disease Molecular biology Enzyme Activation MicroRNAs 030104 developmental biology chemistry UVB-induced apoptosis 030220 oncology & carcinogenesis Cancer research Signal transduction |
| Zdroj: | Biochemical and Biophysical Research Communications. 471:361-367 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2016.02.021 |
| Popis: | Alterations in microRNA-26b (miR-26b) expression have been shown to participate in various malignant tumor developments. However, the possible function of miR-26b in human melanoma cells remains unclarified. In this study, quantitative polymerase chain reaction was used to explore the expression profiles of miR-26b in melanoma cells. The effect of miR-26b on cell viability was determined by using MTT assays and colony formation assay. The apoptosis levels were evaluated by using Annexin V/fluorescein isothiocyanate (FITC) apoptosis detection kit and the apoptosis cells were confirmed by Transmission Electron Microscopy (TEM). Luciferase reporter plasmids were constructed to confirm direct targeting. Our study found that the expression of miR-26b was downregulated in human melanoma specimens. Overexpression of miR-26b significantly increased the anti-proliferative effects and apoptosis in A375 and B16F10 melanoma cells. In addition, luciferase gene reporter assays confirmed that TRAF5 was a direct target gene of miR-26b and the anti-tumor effect of miR-26b in melanoma cells was significantly counteracted by treatment with TRAF5 overexpression. Furthermore, the molecular mechanisms underlying the tumor suppressor of miR-26b in malignant melanomas may be due to the dephosphorylation of MAPK pathway caused by the decrease in TRAF5 expression when miR-26b is up-regulated in melanoma cells. These findings indicate that miR-26b might influence TRAF5-MAPK signaling pathways to facilitate the malignant progression of melanoma cells. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect