Abstract

BackgroundUltraviolet (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.MethodsIn 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.ResultsThe 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.ConclusionsThis 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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.