Yiqi Jiedu Formula inhibits proliferation,invasion and migration of nasopharyngeal carcinoma cells by inhibiting the AKT1/GLUT1 signaling pathway
XU Hongmiao
HE Lan
XIONG Yu
ZOU Fang
LIN Ting
JIANG Zhichao
TANG Le
HE Yingchun
ZHOU Fangliang
Abstract：Objective To investigate the role of the AKT1/GLUT1 signaling pathway in mediating the inhibitory effect of Yiqi Jiedu Formula(YQJDF)against nasopharyngeal carcinoma(NPC)cells.Methods Molecular docking was employed to analyze the binding affinity between the active components of YQJDF and AKT1.MTT assay,real-time cell analysis(RTCA),wound healing assay and Matrigel invasion chamber assay were used to evaluate the effect of YQJDF extract on proliferation,migration and invasion abilities of human NPC cell lines 5-8F and 6-10B,and the changes in cellular protein expression levels were detected using Western blotting.In a BALB/c nude mouse model bearing NPC cell xenografts,tumor growth were observed following treatment with daily gavage with normal saline or YQJDF extract(15.357 g/kg)for 18 consecutive days or with intraperitoneal injections of 5-Fu every other day.The changes in the expressions of AKT1/GLUT1 signaling axis proteins in the xenografts were examined using Western blotting.Results In the NPC cell lines,treatment with YQJDF extract significantly inhibited cell proliferation,migration,and invasion,and downregulated the expressions of p-AKT,GLUT1,XIAP,N-cadherin,and vimentin.The application of GLUT1 or AKT1 activators partially reversed the inhibitory effects of YQJDF on the NPC cells.In the tumor-bearing mouse models,treatment with YQJDF extract obviously suppressed tumor growth and down-regulated the expression of AKT,p-AKT and GLUT1 in the tumor tissues.Conclusion YQJDF inhibits proliferation,invasion,and migration of NPC cells by inhibiting the AKT1/GLUT1 signaling pathway.
Keywords：nasopharyngeal carcinomaYiqi Jiedu FormulaAKT1/GLUT1 signaling pathwayinvasion and migration
Publication Date：2026-02-20
Online Publishing Date：2026-03-04(First online date of this platform, not the publication date of the document)
Pages：12( 259-270 )