Abstract
Introduction miR-199a has been reported as an oncogene of various cancers. However, the biological function and regulatory mechanism of miR-199a in keratinocytes of cholesteatoma are still unclear. Methods Detection by qRT-PCR was conducted on miR-199a's expression in both thirty pairs of cholesteatoma tissues and normal skins. For characterizing the function of miR-199a, this research adopted transwell assay, wound healing assay, and CCK8 assays. Under the support of qRT-PCR, efforts were made to investigate the relative expression of candidate target genes. Moreover, the evaluation of the targeting relationship between miR-199a and the candidate target gene was conducted with the dual-luciferase reporter assay. Results The upregulation of miR-199a was found in cholesteatoma tissues, which facilitated the proliferation, migration, and invasion of HaCaT cells, while its downregulation caused opposite results. Conclusions The findings of the present research offer more insights into the molecular mechanism of cholesteatoma progression.
Highlights
MiR-199a has been reported as an oncogene of various cancers
For the comparison of miR-199a between cholesteatoma and normal retroauricular skin, we collected 30 pairs of cholesteatoma and normal retroauricular skin tissues for later qRT-PCR, finding that miR-199a was significantly upregulated in cholesteatoma tissues compared to the normal retroauricular skin tissues (Figures 1(a)–1(c))
The results of quantitative real-time polymerase chain reaction (qPCR) of the HaCaT cells transfected with miR199a mimics, miR-199a inhibitor, and the negative control are shown in Figures 1(d) and 1(e)
Summary
The biological function and regulatory mechanism of miR-199a in keratinocytes of cholesteatoma are still unclear. The upregulation of miR-199a was found in cholesteatoma tissues, which facilitated the proliferation, migration, and invasion of HaCaT cells, while its downregulation caused opposite results. According to the theoretical mechanism of pathogenesis, middle ear cholesteatoma can be divided into congenital cholesteatoma and acquired cholesteatoma [1]. The former only accounts for 2-4% of all cases and mainly occurs in children aged from 4 to 6 [2]. Despite a large amount of research efforts, the underlying cellular and molecular mechanisms of acquired cholesteatoma remain unclear. It should be noted that keratinocytes are the main cell type of cholesteatoma
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: 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.
