Overexpression of miR-651-5p inhibits ultraviolet radiation-induced malignant biological behaviors of sebaceous gland carcinoma cells by targeting ZEB2

miR-651-5p过表达通过靶向ZEB2抑制紫外线诱导的皮脂腺癌细胞恶性生物学行为

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作者:Haiyan Zhao, Xiaochun Yang, Juan Liu, Fang Han, Zhengrong Yang, Zhongyin Hu, Mingzhi Liu, Yan Mei

Background

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.

Conclusions

This study revealed that overexpression of miR-651-5p inhibited UV-induced SGC growth and metastasis by suppressing ZEB2, which may be a potential target for SGC prevention and therapy.

Methods

In this study, the expression levels of miR-651-5p and zinc finger E-box binding homeobox 2 (ZEB2) 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 ZEB2 were verified by a dual-luciferase reporter assay. An in vivo tumor growth assay was performed to assess tumorigenicity.

Results

The results showed that there was abnormal expression of miR-651-5p and ZEB2 in SGC tissues and cells compared with the control tissues and cells. Overexpression of miR-651-5p and knockdown of ZEB2 inhibited the malignant biological behaviors of SGC cells. Moreover, ZEB2 is one of the target genes of miR-651-5p, and the expression of ZEB2 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 in vitro and in vivo. Conclusions: This study revealed that overexpression of miR-651-5p inhibited UV-induced SGC growth and metastasis by suppressing ZEB2, which may be a potential target for SGC prevention and therapy.

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