Knockout of the histone methyltransferase NSD1 leads to a decrease in cell proliferation and an increase in sensitivity to cisplatin in laryngeal squamous cell carcinoma

Introduction . The histone methylation regulates gene expression and plays a role in genomic stability participating DNA repair. Dimethylation of 3 lysine 36 (H3K36me 2 ) is an important modification which responsible for activation. H3K36me product methyltransferase activity NSD1, NSD2, NSD3, ASH1L proteins. NSD1 mutations are known to often occur head neck squamous carcinoma. presence highly correlates with increased survival, especially patients laryngeal cancer. aim this study was vitro investigation the cell proliferation cancer non-small lung cells, as well effect disruption on cisplatin treatment response. Material Methods Using TCGA, correlation analysis performed compare wild type mutant patient survival. knockout lines models were developed using CRISPR/ Cas9 system. H3K36me2 level evaluated by western blot. Proliferation IC50 control cells studied well. Results It demonstrated that decreased sensitivity treatment, while there no line. Conclusion Based data obtained, it can be concluded NS D 1 protein potential target inhibitor development following vivo testing head-neck carcinoma models. More studies needed better understanding regulation tumor growth