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甲基化转移酶SETDB1对口腔鳞状癌细胞 迁移侵袭能力的影响及其机制.
- Source :
-
Shandong Medical Journal . 6/15/2024, Vol. 64 Issue 17, p21-24. 4p. - Publication Year :
- 2024
-
Abstract
- Objective To observe the effect of methyltransferase SETDB1 on the migration and invasion of oral squamous cell carcinoma cells, and to explore the related mechanisms. Methods Different concentrations of methyltransferase inhibitors GSK3685032 (0,0. 2,0. 4,0. 6,0. 8 µmol/L) acted on the oral squamous cell carcinoma CAL-27 cells. Cell proliferative viability was measured by the MTT method, and we found that the optimal action concentration of GSK3685032 was 0. 6 µmol/L. CAL-27 cells were divided into the control and experimental groups; cells in the control group were treated with organic solvent DMSO, and cells in the experimental group were treated with 0. 6 µmol/L GSK3685032. Cell SETDB1 mRNA was measured by RT-qPCR, and the SETDB1 protein was detected by Western blotting. Cell migration ability was detected by Scratch assay, the invasion ability was detected by Transwell chamber invasion assay, and SOX 7 methylation level was tested by pyrosequencing. Results The mRNA and protein expression levels of SETDB1 were lower in the experimental group than in the control group (both P<0. 05). The migration distance of the experimental group was less than that of the control group, and the number of transmenbrance cells was smaller than that of the control group (P<0. 05). The methylation rate of SOX 7 in the experimental group was lower than that of the control group (P<0. 05). Conclusion Methyltransferase SETDB1 can inhibit the migration and invasion of oral squamous cell carcinoma cells, and the mechanism may be related to the down-regulation of intracellular SOX7 methylation level. [ABSTRACT FROM AUTHOR]
Details
- Language :
- Chinese
- ISSN :
- 1002266X
- Volume :
- 64
- Issue :
- 17
- Database :
- Academic Search Index
- Journal :
- Shandong Medical Journal
- Publication Type :
- Academic Journal
- Accession number :
- 178054551
- Full Text :
- https://doi.org/10.3969/j.issn.1002-266X.2024.17.005