Abstract
MicroRNAs (miRNAs/miRs) are small non-coding RNAs that can act as oncogenes or tumor-suppressor genes in human cancer. Previous studies have revealed that abnormal expression of miRNAs is closely associated with tumor cell cycle, differentiation, growth and apoptosis. miR-543 is expressed abnormally in a wide variety of cancers and has been associated with cellular proliferation, apoptosis, and invasion; however, the effect of miR-543 remains unknown in oral squamous cell carcinoma (OSCC). In the present study, the expression level of miR-543 in OSCC cell lines and tissues was investigated by RT-qPCR. A series of experiments was then performed to elucidate the functions of miR-543 in OSCC, such as CCK-8 assay, colony formation assay, flow cytometry, cell cycle distribution assay and cell apoptosis assay and Transwell assay. miR-543 expression was significantly upregulated in tumors from patients with OSCC and in OSCC cell lines. Overexpression of miR-543 promoted the proliferation, invasion and migration of OSCC cell lines, and inhibited cell apoptosis. In addition, the present study identified cytochrome P450 family 3 subfamily A member 5 (CYP3A5) as a direct target of miR-543 using software analysis and dual-luciferase reporter assays. In conclusion, the results of the present study suggest that miR-543 acts as a tumor promoter and serves a vital role in OSCC proliferation and invasion. These results confirm that miR-543 may serve as a potential novel target for the treatment of OSCC.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
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.