BioMed research international · 2021
miR-199a Targeting PNRC1 to Promote Keratinocyte Proliferation and Invasion in Cholesteatoma.
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Yao Lihui, Zhang Wenjing, Zheng Jian, Lu Xing, Zhang Fan
Аннотация
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.
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.