Background: Melanoma is an extremely aggressive malignant skin tumor with high mortality. Many types of long noncoding RNAs and microRNAs have been reported to be associated with the oncogenesis of melanoma. However, a novel lncRNA-NEAT has not been thoroughly investigated in melanoma cancer. The purposes of this study were to investigate the underlying molecular mechanism in a novel couple of lnc-NEAT1 and miR-23a-3p, as well as the function role of KLF3 in the regulation of melanoma cancer.
Methods: 28 groups of tumor tissues and normal tissues were obtained from melanoma cancer patients. We performed a series of experiments and analysis, including RT-qPCR, western blots, CCK-8 assay, and migration/invasion assay, to investigate the expressions of NEAT1, miR-23a-5p and KLF3, cell viabilities, and tumor growth in vivo.
Results: In this study, we observed that the expression of NEAT1 was significantly upregulated in melanoma tissues, which remarkedly promoted the cells' proliferation, cell migration, and invasion in melanoma cell lines. Besides, NEAT1 could directly bind to miR-23a-3p, which was found to reverse the effect caused by NEAT1. MiR-23a-3p was discovered to bind to 3'UTR of KLF3, which reduced KLF3 expression. In addition, the overexpression of KLF3 could lower the effects of miR-23a-3p caused on melanoma cancer cell development.
Conclusion: Our results demonstrated that NEAT1 could sponge miR-23a-3p and functions via the expression of KLF3. This axis of NEAT1/miR-23a-5p/KLF3 could together regulate melanoma cancer proliferation. This might provide a new therapeutic strategy for melanoma skin cancer.Trial registration HBTCM38574839, registered 12 October 2012.
Keywords: KLF3; Melanoma cancer; NEAT1; miR-23a-3p.