S1PR1通过p-STAT1/miR-30c-5 p/FOXA1路径抑制肺腺癌的进展
Yanfei Chai1,2,3, Hong Xiang1,4, Yuchao Ma2
1Department of Health Management Center, The Third Xiangya Hospital of Central South University, Changsha, China.
Journal of experimental & clinical cancer research : CR
|November 17, 2024
概括
斯芬戈辛-1-酸盐受体1 (S1PR1) 在肺腺癌 (LUAD) 中被下调,抑制癌症的进展. 通过调节miR-30c-5p/FOXA1通路,S1PR1抑制瘤生长,改善患者的预后.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 肺腺癌 (LUAD) 的进展与神素-1-酸盐受体1 (S1PR1) 有关,但其确切的作用尚不清楚.
- 研究S1PR1的功能和LUAD下游途径对于理解瘤发生至关重要.
研究的目的:
- 阐明S1PR1在LUAD中的作用和分子机制.
- 为了确定由S1PR1在LUAD进展中调节的下游信号通路.
主要方法:
- 生物信息学,RT-qPCR,Western blot和IHC评估了LUAD中的S1PR1表达和预后.
- 功能性测试 (CCK-8,殖民地形成,迁移,入侵,粘附) 评估了S1PR1对LUAD细胞的影响.
- 通过RNA测序,KEGG,GO,GSEA,ChIP和双光酶记者测定,确定了S1PR1受调的途径和点,包括FOXA1和miR-30c-5p.
主要成果:
- 在LUAD中S1PR1的表达下降,并且与患者的预后有积极的相关性.
- 通过减少COL5A1,MMP1和SERPINE1的表达,S1PR1过度表达抑制了LUAD细胞的增殖,迁移,入侵和粘附.
- S1PR1通过p-STAT1/miR-30c-5p轴抑制FOXA1的表达,从而抑制LUAD恶性瘤.
结论:
- 在LUAD中S1PR1的下调与更差的预后有关.
- S1PR1通过p-STAT1/miR-30c-5p/FOXA1信号通路抑制COL5A1,MMP1和SERPINE1,从而抑制LUAD细胞恶性瘤.
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