Effect of methyltransferase SETDB1 on migration and invasion of oral cancer cells and its mechanism
HAO Yan
BAI Xiangyu
HUO Feng
CHEN Xibo
Abstract:Objective To observe the effect of methyltransferase SETDB1 on the migration and invasion of oral squa-mous cell carcinoma cells,and to explore the related mechanisms.Methods Different concentrations of methyltransfer-ase 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 blot-ting.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 ex-perimental 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.
Keywords:methyltransferaseSETDB1methyltransferase inhibitorSOX7oral carcinomaoral squamous cell carcinoma
Publication Date:2024-06-15
Online Publishing Date:2025-08-15(First online date of this platform, not the publication date of the document)
Pages:4( 21-24 )
Shandong Medical Journal

Shandong Medical Journal

ISTIC
ISSN:1002-266X
Year, Vol.(Issue):2024,64(17)