Zhao Haiyan, Yang Xiaochun, Liu Juan, Han Fang, Yang Zhengrong, Hu Zhongyin, Liu Mingzhi, Mei Yan
Faculty of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming, China.
Department of Ophthalmology, The Affiliated Hospital of Kunming University of Science and Technology, The First People's Hospital of Yunnan Province, Kunming, China.
Ann Transl Med. 2022 May;10(9):517. doi: 10.21037/atm-21-3897.
Ultraviolet (UV) exposure is the most essential etiological factor in sebaceous gland carcinoma (SGC). The abnormal expression of microRNAs (miRNAs) is also involved in SGC. However, the function of miRNAs in UV-induced SGC is still unclear.
In this study, the expression levels of miR-651-5p and zinc finger E-box binding homeobox 2 () in SGC tissues and cells were measured by real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting. Then, the effects of miR-651-5p on the apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) of UV-induced SGC cells were determined. The interactions between miR-651-5p and were verified by a dual-luciferase reporter assay. An tumor growth assay was performed to assess tumorigenicity.
The results showed that there was abnormal expression of miR-651-5p and in SGC tissues and cells compared with the control tissues and cells. Overexpression of miR-651-5p and knockdown of inhibited the malignant biological behaviors of SGC cells. Moreover, is one of the target genes of miR-651-5p, and the expression of was negatively regulated by miR-651-5p in SGC cells. Further studies showed that overexpression of miR-651-5p promoted cell apoptosis and inhibited the cell invasion and migration ability and EMT of UV-induced SGC cells by downregulating the expression of ZEB2 and .
This study revealed that overexpression of miR-651-5p inhibited UV-induced SGC growth and metastasis by suppressing , which may be a potential target for SGC prevention and therapy.
紫外线(UV)暴露是皮脂腺癌(SGC)最主要的病因。微小RNA(miRNA)的异常表达也与SGC有关。然而,miRNA在紫外线诱导的SGC中的功能仍不清楚。
在本研究中,通过实时定量聚合酶链反应(RT-qPCR)和蛋白质印迹法检测SGC组织和细胞中miR-651-5p和锌指E盒结合同源框2(ZEB2)的表达水平。然后,确定miR-651-5p对紫外线诱导的SGC细胞凋亡、迁移、侵袭和上皮-间质转化(EMT)的影响。通过双荧光素酶报告基因检测验证miR-651-5p与ZEB2之间的相互作用。进行皮下肿瘤生长试验以评估致瘤性。
结果显示,与对照组织和细胞相比,SGC组织和细胞中miR-651-5p和ZEB2存在异常表达。miR-651-5p的过表达和ZEB2的敲低抑制了SGC细胞的恶性生物学行为。此外,ZEB2是miR-651-5p的靶基因之一,在SGC细胞中,miR-651-5p负调控ZEB2的表达。进一步研究表明,miR-651-5p的过表达通过下调ZEB2的表达促进细胞凋亡,并抑制紫外线诱导的SGC细胞的侵袭和迁移能力以及EMT。
本研究表明,miR-651-5p的过表达通过抑制ZEB2抑制紫外线诱导的SGC生长和转移,这可能是SGC预防和治疗的潜在靶点。