Cutaneous malignant melanoma, whose incidence is increasing steadily worldwide, is the result of complex interactions between individual genetic factors and environmental risk factors.,Ultraviolet radiation represents the most important environmental risk factor for the development of skin cancers, including melanoma.,Sun exposure and early sunburn during childhood are the principal causes of cutaneous melanoma insurgence in adults, with double the risk relative to a nonexposed population.,Consequently, ultraviolet protection has long been recognized as an important measure to prevent such a malignancy.,Biological and epidemiological data suggest that vitamin D status could affect the risk of cancer and play a role in cancer prevention by exerting antiproliferative effects.,Solar radiations are critical for vitamin D synthesis in humans; however, uncontrolled and intensive sun exposure is dangerous to skin health and may contribute toward the development of cutaneous malignant melanoma.,An optimum balance between sun protection and exposure is thus advocated.,Additional research is required to confirm the preventive role of vitamin D in melanoma incidence or a positive influence on patient outcome.
MicroRNAs (miRNAs) are attractive therapeutic targets for various therapy-resistant tumors.,However, the association between miRNA and BRAF inhibitor resistance in melanoma remains to be elucidated.,We used microarray analysis to comprehensively study the miRNA expression profiling of vemurafenib resistant (VemR) A375 melanoma cells in relation to parental A375 melanoma cells.,MicroRNA-7 (miR-7) was identified to be the most significantly down-regulated miRNA in VemR A375 melanoma cells.,We also found that miR-7 was down-regulated in Mel-CVR cells (vemurafenib resistant Mel-CV melanoma cells).,Reestablishment of miR-7 expression could reverse the resistance of both cells to vemurafenib.,We showed that epidermal growth factor receptor (EGFR), insulin-like growth factor-1 receptor (IGF-1R) and CRAF were over-expressed in VemR A375 melanoma cells.,Introduction of miR-7 mimics could markedly decrease the expressions of EGFR, IGF-1R and CRAF and further suppressed the activation of MAPK and PI3K/AKT pathway in VemR A375 melanoma cells.,Furthermore, tumor growth was inhibited in an in vivo murine VemR A375 melanoma tumor model transfected with miR-7 mimics.,Collectively, our study demonstrated that miR-7 could reverse the resistance to BRAF inhibitors in certain vemurafenib resistant melanoma cell lines.,It could advance the field and provide the basis for further studies in BRAF inhibitor resistance in melanoma.