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논문 기본 정보

자료유형
학술저널
저자정보
Zhao Haoliang (Orthopedics Department Shanxi Bethune Hospital Shanxi Academy Of Medical Sciences P.R. China) Zhang Ming (Orthopedics Department Shanxi Bethune Hospital Shanxi Academy Of Medical Sciences P.R. China) Yang Xuejing (Cancer Center Shanxi Bethune Hospital Shanxi Academy Of Medical Sciences P.R. China) Song Dong (Cancer Center Shanxi Bethune Hospital Shanxi Academy Of Medical Sciences P.R. China)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제31권 제10호
발행연도
2021.10
수록면
1,331 - 1,342 (12page)
DOI
10.4014/jmb.2106.06028

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In this study, we evaluated the mechanism of long non-coding RNA MIR22 host gene (LncRNA MIR22HG) in osteosarcoma cells. Forty-eight paired osteosarcoma and adjacent tissues samples were collected and the bioinformatic analyses were performed. Target genes and potential binding sites of MIR22HG, microRNA (miR)-629-5p and tet methylcytosine dioxygenase 3 (TET3) were predicted by Starbase and TargetScan V7.2 and confirmed by dual-luciferase reporter assay. Cell Counting Kit-8, colony formation and flow cytometry assays were utilized to determine the viability, proliferation and apoptosis of transfected osteosarcoma cells. Pearson’s analysis was introduced for the correlation analysis between MIR22HG and miR-629-5p in osteosarcoma tissue. Relative expressions of MIR22HG, miR-629-5p and TET3 were measured by quantitative real-time polymerase chain reaction or Western blot. MiR-629-5p could competitively bind with and was negatively correlated with MIR22HG, the latter of which was evidenced by the high expression of miR-629-5p and low expression of MIR22HG in osteosarcoma tissues. Overexpressed MIR22HG repressed the viability and proliferation but enhanced apoptosis of osteosarcoma cells, which was reversed by miR-629-5p upregulation. TET3 was the target gene of miR-629-5p, and the promotive effects of upregulated miR-629-5p on the viability and proliferation as well as its repressive effect on apoptosis were abrogated via overexpressed TET3. To sum up, overexpressed MIR22HG inhibits the viability and proliferation of osteosarcoma cells, which was achieved via regulation of the miR-629- 5p/TET3 axis.

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