SLC4A3 Promotes Glioblastoma Growth and Epithelial-mesenchymal Transformation by Regulating the NF-κB Signaling Pathway
10.11969/j.issn.1673-548X.2025.03.009
- VernacularTitle:SLC4A3通过调控NF-κB信号通路促进胶质母细胞瘤的生长和上皮间质转化
- Author:
Gong CHENG
1
;
Lun GAO
;
Junhui LIU
Author Information
1. 433200 洪湖市人民医院重症医学科
- Publication Type:Journal Article
- Keywords:
SLC4A3;
GBM;
Proliferation;
EMT;
NF-κB signaling pathway
- From:
Journal of Medical Research
2025;54(3):40-46
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the biological function and molecular mechanism of solute carrier family 4,member 3(SLC43)in glioblastoma(GBM).Methods The expression difference of SLC4A3 in 30 GBM and 10 normal brain tissues were analyzed by immu-nohistochemistry.Kaplan-Meier survival analysis was used to evaluate the effect of SLC4A3 on the prognosis of GBM patients.The ex-pression of SLC4A3 in U87 and U251 cells was reduced by shRNA,and the changes in the proliferation,migration and invasion ability of GBM cells were detected after the knockdown,and Western blot was used to investigate the expression of epithelial-mesenchymal transi-tion(EMT)and NF-κB signaling pathway related proteins after SLC4A3 knockdown.Results SLC4A3 was overexpressed in GBM,and high expression of SLC4A3 was associated with poor prognosis.Knocking down SLC4A3 inhibited the proliferation,migration and in-vasion of U87 and U251 cells,and the expression levels of N-cadherin and Vimentin were down-regulated,while the expression levels of E-cadherin were increased.In addition,knocking down SLC4A3 inhibited the NF-κB signaling pathway and further found that nu-clear translocation of NF-κB p65 was inhibited.Conclusion SLC4A3mediates the NF-κB signaling pathway by regulating the nuclear translocation of NF-κB p65 to influence the growth and EMT of GBM cells,which is a novel prognostic biomarker for GBM.
