Wang Zhengxiang, Liu Yaling
Department of Dermatology, Hebei Medical University, Shijiazhuang, Hebei 050030, P.R. China.
Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050031, P.R. China.
Oncol Lett. 2021 Feb;21(2):88. doi: 10.3892/ol.2020.12349. Epub 2020 Dec 6.
The aim of the present study was to determine the impact of microRNA (miRNA/miR)-633 on the biological properties of malignant melanoma cells. Kang-Ai 1 (KAI1), also known as cluster of differentiation 82, is an important transcriptional regulator and tumor suppressor gene present in different types of tumors. miRNAs that potentially bind with KAI1 were predicted via bioinformatics analyses. In total, six putative miRNA regulators of KAI1 were identified in the present analysis, among which miR-633 was upregulated the most in melanoma tissues compared with the control group. The expression levels of miR-633 and KAI1 in melanoma tissues compared with adjacent normal tissues were then assessed. It was found that miR-633 was significantly upregulated in melanoma cells compared with the control group, whereas the expression levels of KAI1 showed the opposite results. miR-633 was predicted to target the 3'-untranslated region of KAI1 using predictive online tools, and results from luciferase reporter assays confirmed the direct regulation of KAI1 promoter activity by miR-633. Furthermore, miR-633 mimics over expression was shown to suppress both mRNA and protein expression of KAI1, while miR-633 inhibition resulted in decreased viability and migrationin melanoma cells . Taken together, the present study demonstrated, to the best of the authors' knowledge for the first time, that miR-633 exerts an important role in melanoma through targeting KAI1.
本研究的目的是确定微小RNA(miRNA/miR)-633对恶性黑色素瘤细胞生物学特性的影响。康艾1(KAI1),也称为分化簇82,是一种重要的转录调节因子和肿瘤抑制基因,存在于不同类型的肿瘤中。通过生物信息学分析预测了可能与KAI1结合的miRNA。在本分析中,总共鉴定出6个假定的KAI1 miRNA调节因子,其中与对照组相比,miR-633在黑色素瘤组织中上调最为明显。然后评估了黑色素瘤组织与相邻正常组织中miR-633和KAI1的表达水平。结果发现,与对照组相比,黑色素瘤细胞中miR-633显著上调,而KAI1的表达水平则相反。使用在线预测工具预测miR-633靶向KAI1的3'-非翻译区,荧光素酶报告基因检测结果证实miR-633直接调节KAI1启动子活性。此外,miR-633模拟物过表达可抑制KAI1的mRNA和蛋白表达,而抑制miR-633则导致黑色素瘤细胞活力和迁移能力下降。综上所述,据作者所知,本研究首次证明miR-633通过靶向KAI1在黑色素瘤中发挥重要作用。