Abstract
BackgroundMelanoma 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.Methods28 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.ResultsIn 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.ConclusionOur 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
Highlights
Melanoma is an extremely aggressive malignant skin tumor with high mortality
Our results found that in melanoma skin cancer (i) NEAT1 was over-expressed, and it promoted cell proliferation, migration, and invasion; (ii) expression of miR23a-3p was inhibited by NEAT1; (iii) the sponge between NEAT1 and miR-23a-3p could regulate melanoma proliferation; and (iv) MiR-23a-3p targeted Krüppel-like factor 3 (KLF3) and NEAT1/ miR-23a axis regulated melanoma proliferation, migration, and invasion via KLF3
NEAT1 is overexpressed in human melanoma tissues We evaluated the expressions of NEAT1 in 28 groups of melanoma cancer tissues and their adjacent normal tissues by RT-PCR
Summary
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. 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. Scientists have revealed the long-non-coding RNAs, lncRNAs, are playing important roles in tumorigenesis development or NEAT1, nuclear enriched abundant transcript 1, is a novel lncRNA, transcribed from multiple endocrine neoplasia locus [8, 9, 12,13,14,15,16,17]. There is a growing interest in the structural role of this novel lncRNA-NEAT1 in other types of cancers, for example, in melanoma skin cancer
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