Study on the mechanism of PRMT1 regulating the proliferation, apoptosis and migration of oral squamous cell carcinoma SCC-25 cells

CHEN Qian; CUI Wen-juan

doi:10.11659/jjssx.01E025118

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Study on the mechanism of PRMT1 regulating the proliferation, apoptosis and migration of oral squamous cell carcinoma SCC-25 cells

Basic Research | 更新时间：2025-10-24

- Study on the mechanism of PRMT1 regulating the proliferation, apoptosis and migration of oral squamous cell carcinoma SCC-25 cells
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 34, Issue 10, Pages: 855-860(2025)
- 作者机构：
  
  上海市第八人民医院口腔科，上海 200235
- 作者简介：
- 基金信息：
- DOI：10.11659/jjssx.01E025118
  CLC： R78;R73
- Received：22 January 2025，
  
  Published：25 October 2025
- 稿件说明：
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陈钱,崔文娟.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[J].局解手术学杂志,2025,34(10):855-860.

CHEN Qian,CUI Wen-juan.Study on the mechanism of PRMT1 regulating the proliferation, apoptosis and migration of oral squamous cell carcinoma SCC-25 cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(10):855-860.
陈钱,崔文娟.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[J].局解手术学杂志,2025,34(10):855-860. DOI： 10.11659/jjssx.01E025118.

CHEN Qian,CUI Wen-juan.Study on the mechanism of PRMT1 regulating the proliferation, apoptosis and migration of oral squamous cell carcinoma SCC-25 cells[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(10):855-860. DOI： 10.11659/jjssx.01E025118.

摘要

目的

探讨蛋白质精氨酸甲基转移酶1（PRMT1）在调控人口腔鳞状细胞癌细胞SCC-25增殖、凋亡、迁移过程中的作用和潜在机制。

方法

收集并培养正常口腔黏膜细胞S-G及口腔鳞状细胞癌细胞SCC-25、OECM-1、HSC-3，检测PRMT1的转录水平。将SCC-25细胞分为未转染组（SCC-25组）、空载体对照组（SCC-25+NC组）和转染组（SCC-25+si-PRMT1组）。使用Western blot检测蛋白表达水平；通过MTT及细胞划痕实验分别检测细胞的增殖和迁移能力；利用流式细胞仪检测细胞凋亡率。在构建的SCC-25+si-PRMT1细胞基础上进行外源性TGF-β刺激实验，以验证TGF-β/Smad通路在PRMT1沉默效应中的作用。

结果

与正常口腔黏膜细胞S-G相比，PRMT1在口腔鳞状细胞癌细胞SCC-25、OECM-1、HSC-3中均呈高表达（

0.05），且在SCC-25细胞中表达最为显著（

0.05）。PRMT1基因沉默后，SCC-25细胞内促凋亡蛋白Bax、C-Caspase-3表达显著增加，细胞凋亡率显著上升，抗凋亡蛋白Bcl-2表达显著降低，细胞增殖和迁移能力受到抑制；同时沉默PRMT1基因可显著降低TGF-β及其下游p-Smad的表达水平。与SCC-25+si-PRMT1组相比，SCC-25+si-PRMT1+TGF-β组细胞增殖与迁移能力增强，凋亡率下降，提示TGF-β可部分逆转PRMT1沉默所致的抑癌效应。

结论

PRMT1通过调控TGF-β/Smad信号通路调节SCC-25细胞的增殖、凋亡和迁移过程。

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 （

0.05）， with the highest expression observed in SCC-25 cells （

0.05）. After silencing the PRMT1 gene， the expressions of pro-apoptotic proteins B

ax 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.

关键词

Keywords

references

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