miR-767-3p suppresses melanoma progression by inhibiting ASF1B expression

Melanoma, the type of skin cancer considered as most malignant, and known to be linked with a high incidence as well as high mortality rate. Although the dysregulation of ASF1B and miR-767-3p expression is involved in the progression of various cancers, their biological function in melanoma remains unclear. Real-time qPCR was the primary source for determining the levels of ASF1B and miR-767-3p in melanoma. For the validation of association among miR-767-3p and ASF1B, luciferase activity assay was used. Quantification of cell apoptosis, proliferation, migration and viability in melanoma cells were carried out by flow cytometry, BrdU, transwell assays, and CCK-8, respectively. Further evaluation of tumor growth was achieved by xenograft in vivo. Results showed an increased expression of ASF1B while declined expression of miR-767-3p in melanoma. ASF1B knockdown repressed cell migration, viability, proliferation, and tumor growth whereas boosted apoptosis in A375 as well as in A875 melanoma cells. Moreover, miR-767-3p attenuated the migration and proliferation of melanoma cells and encouraged cell apoptosis by reducing ASF1B levels. In this study, miR-767-3p was shown to inhibit ASF1B which will attenuate melanoma tumorigenesis, and by this it can be a potential new effective biomarker for the treatment of melanoma. •ASF1B is identified as the miR-767-3p downstream effector.•ASF1B was obviously increased in melanoma.•ASF1B knockdown inhibited tumor growth of melanoma in vivo.•ASF1B accelerated the progression of melanoma cells.