MicroRNA-373 promotes cell migration via targeting salt-inducible kinase 1 expression in melanoma
MicroRNA-373 promotes cell migration via targeting salt-inducible kinase 1 expression in melanoma
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DOI：
10.3892/etm.2018.6784
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发表时间：
2018-12-01
影响因子：
2.7
通讯作者：
Xu, Yi
中科院分区：
文献类型：
--
作者：
Bai, Xinping;Yang, Ming;Xu, Yi
众所周知，微小RNA（miR）的表达改变在许多人类癌症类型中至关重要。然而，许多miR的分子机制尚未阐明。在本研究中，进行逆转录-定量聚合酶链反应和蛋白质印迹分析，以及细胞迁移试验，以验证miR-373在黑色素瘤中的失调及其生物学功能。与痣和正常黑素细胞相比，miR-373的转录水平在黑素瘤组织和细胞系中被鉴定为上调。miR-373被鉴定为作为oncomiR起作用，促进黑色素瘤细胞迁移。值得注意的是，观察到miR-373通过直接结合SIK 1表达的3-非翻译区来抑制其下游基因盐诱导激酶1（SIK 1）。此外，SIK 1表达减少被鉴定为是miR-373的致癌作用的原因。总之，本研究表明miR-373作为oncomiR通过靶向SIK 1表达促进黑色素瘤进展。这可能为黑色素瘤的治疗提供新的途径。
It is well established that altered expression of microRNAs (miRs) is critical in numerous human cancer types. Nevertheless, the molecular mechanisms of many miRs are yet to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction and western blot analyses, and cell migration assays were performed to verify dysregulation of miR-373 in melanoma and its biological function. The transcriptional level of miR-373 was identified to be upregulated in melanoma tissues and cell lines compared with nevus and normal melanocytes. miR-373 was identified to function as an oncomiR, promoting melanoma cell migration. Notably, miR-373 was observed to suppress its downstream gene salt-inducible kinase 1 (SIK1) through directly binding the 3-untranslated region of SIK1 expression. Furthermore, reduced SIK1 expression was identified to be responsible for the oncogenic effect of miR-373. In conclusion, the present study indicates that miR-373 functions as an oncomiR to promote melanoma progression through targeting SIK1 expression. This may provide a new therapeutic approach for melanoma.