Study on the mechanism of PRMT1 regulating the proliferation,apoptosis and migration of oral squamous cell carcinoma SCC-25 cells
- VernacularTitle:PRMT1调控口腔鳞状细胞癌SCC-25细胞增殖、凋亡与迁移的机制研究
- Author:
Qian CHEN
1
;
Wen-juan CUI
1
Author Information
- Publication Type:Journal Article
- Keywords: protein arginine methyltransferase 1; oral squamous cell carcinoma; TGF-β/Smad signaling pathway
- From: Journal of Regional Anatomy and Operative Surgery 2025;34(10):855-860
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the role and potential mechanism of protein arginine methyltransferase 1(PRMT1)in regulating the proliferation,apoptosis and migration of human oral squamous cell carcinoma SCC-25 cells.Methods Normal oral mucosal cells S-G and oral squamous cell carcinoma cells SCC-25,OECM-1,and HSC-3 were collected and cultured,and the transcription level of PRMT1 was detected.SCC-25 cells were divided into the untransfected group(SCC-25 group),empty vector control group(SCC-25+NC group),and transfection group(SCC-25+si-PRMT1 group).Protein expression levels were detected by Western blot;cell proliferation and migration abilities were assessed by MTT assay and cell scratch wound healing assay,respectively;and the apoptosis rates were determined by flow cytometry.Exogenous TGF-β stimulation experiment was conducted on the basis of constructed SCC-25+si-PRMT1 cells to verify the role of TGF-β/Smad pathway in the PRMT1 silencing effect.Results Compared with normal oral mucosal cells S-G,PRMT1 was highly expressed in oral squamous cell carcinoma cells SCC-25,OECM-1,and HSC-3(P<0.05),with the highest expression observed in SCC-25 cells(P<0.05).After silencing the PRMT1 gene,the expressions of pro-apoptotic proteins Bax and C-Caspase-3 in SCC-25 cells significantly increased,the apoptosis rate significantly increased,the expression of anti-apoptotic protein Bcl-2 significantly decreased,and the cell proliferation and migration abilities were inhibited.Simultaneous silencing of the PRMT1 gene can significantly downregulated the expression levels of TGF-β and its downstream effector p-Smad.Compared with the SCC-25+si-PRMT1 group,the cell proliferation and migration abilities in the SCC-25+si-PRMT1+TGF-β group were enhanced,and the apoptosis rate decreased,which suggesting that TGF-β could partially reverse the tumor suppressor effect caused by PRMT1 silencing.Conclusion PRMT1 regulates the proliferation,apoptosis and migration of SCC-25 cells through TGF-β/Smad signaling pathway.
