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微小RNA-27b通过靶向MYC抑制黑色素瘤的发展。

MicroRNA-27b inhibits the development of melanoma by targeting MYC.

作者信息

Tian Yi, Zeng Juanni, Yang Zongliang

机构信息

Department of Dermatology, The Second Affiliated Hospital, Hunan University of Chinese Medicine, Changsha, Hunan 410005, P.R. China.

Department of Anorectal Disease, The Second Affiliated Hospital, Hunan University of Chinese Medicine, Changsha, Hunan 410005, P.R. China.

出版信息

Oncol Lett. 2021 May;21(5):370. doi: 10.3892/ol.2021.12631. Epub 2021 Mar 12.

Abstract

Cutaneous malignant melanoma is a malignancy with one of the fastest increasing incidence rates worldwide; however, the mechanism underlying the occurrence and development of melanoma remains unclear. The aim of the present study was to identify novel biomarkers for the occurrence and development of melanoma. The results of the present study demonstrated that the expression levels of microRNA (miR)-27b were decreased in melanoma tissue samples compared with those in adjacent noncancerous tissue samples and cells according to online and experimental data. By contrast, MYC expression levels were upregulated in melanoma compared with those in adjacent noncancerous tissue samples. miR-27b overexpression significantly inhibited A375 and A2085 melanoma cell DNA synthesis, viability and invasive ability. Dual-luciferase reporter assay results demonstrated that miR-27b inhibited MYC expression through binding to the 3'-untranslated region of MYC mRNA. MYC knockdown in melanoma cells exerted similar effects to those of miR-27b overexpression on DNA synthesis, cell viability and invasive ability; the effects of miR-27b inhibition were significantly reversed by MYC knockdown. In conclusion, the miR-27b/MYC axis may modulate malignant melanoma cell biological behaviors and may be a potential target for melanoma treatment.

摘要

皮肤恶性黑色素瘤是一种在全球发病率增长最快的恶性肿瘤之一;然而,黑色素瘤发生和发展的潜在机制仍不清楚。本研究的目的是鉴定黑色素瘤发生和发展的新型生物标志物。根据在线和实验数据,本研究结果表明,与相邻非癌组织样本和细胞相比,黑色素瘤组织样本中微小RNA(miR)-27b的表达水平降低。相比之下,与相邻非癌组织样本相比,黑色素瘤中MYC的表达水平上调。miR-27b过表达显著抑制A375和A2085黑色素瘤细胞的DNA合成、活力和侵袭能力。双荧光素酶报告基因检测结果表明,miR-27b通过与MYC mRNA的3'非翻译区结合来抑制MYC表达。黑色素瘤细胞中的MYC敲低对DNA合成、细胞活力和侵袭能力产生了与miR-27b过表达类似的影响;MYC敲低显著逆转了miR-27b抑制的作用。总之,miR-27b/MYC轴可能调节恶性黑色素瘤细胞的生物学行为,可能是黑色素瘤治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0689/7967934/1ab93d0af1e6/ol-21-05-12631-g00.jpg

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