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. 2022 Feb;477(2):537-547.
doi: 10.1007/s11010-021-04301-3. Epub 2021 Nov 26.

MiR-196a promotes the proliferation and migration of esophageal cancer via the UHRF2/TET2 axis

Chang-Mei Hu  1 , Jie Peng  2 , Liang Lv  3 , Xue-Hong Wang  3 , Ji-Rong Huo  3 , De-Liang Liu  3
Affiliations

MiR-196a promotes the proliferation and migration of esophageal cancer via the UHRF2/TET2 axis

Chang-Mei Hu et al. Mol Cell Biochem. 2022 Feb.

Abstract

The aim of this study was to investigate the functions and molecular mechanism of miR-196a in esophageal cancer (EC). miR-196a as well as UHRF2 and TET2 mRNA and protein levels in EC tissues and cells were detected using quantitative real-time PCR or western blot, respectively. Cell proliferation was evaluated via MTT assay. Transwell assays were used to detect cell migration. In addition, the targeted relationship between miR-196a and UHRF2 was assessed through a dual luciferase reporter assay. Enzyme-linked immunosorbent assay was performed to detect the levels of the cytosine intermediates 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). We found increased miR-196a expression in EC tissues and cells but decreased UHRF2 and TET2 expression. Next, functional experiments showed that knockdown of miR-196a or UHRF2 overexpression suppress EC cell proliferation and migration. miR-196a negatively regulates TET2 expression by directly targeting UHRF2. UHRF2 overexpression decreased 5mC levels but increased 5hmC levels. Furthermore, TET2 downregulation reversed the functions of miR-196a inhibition on EC cell proliferation and migration. Collectively, our study suggested that miR-196a was closely related to the progression of EC possibly by regulating the UHRF2/TET2 axis. Thus, miR-196a represents a potential new EC therapeutic target.

Keywords: Esophageal cancer; Proliferation and migration; TET2; UHRF2; miR-196a.

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