Shenqi Yiliu Prescription Reverses Cisplatin Resistance in Ovarian Cancer Cells by Regulating PI3K/Akt/mTOR Signaling Pathway-mediated Glycolysis
10.13422/j.cnki.syfjx.20251121
- VernacularTitle:基于PI3K/Akt/mTOR信号通路调控糖酵解探讨参芪抑瘤方逆转卵巢癌细胞顺铂耐药的作用机制
- Author:
Lan MA
1
;
Yuping YANG
2
;
Min BAI
3
;
Yongqiang DUAN
3
;
Zhining ZHANG
1
Author Information
1. General Hospital of Ningxia Medical University，Yinchuan 750004，China
2. School of Clinical Chinese Medicine，Gansu University of Chinese Medicine，Lanzhou 730000，China
3. Key Laboratory of Ningxia Minority Medicine Modernization Ministry of Education， Ningxia Medical University，Yinchuan 750004，China
- Publication Type:Journal Article
- Keywords:
ovarian cancer;
Shenqi Yiliu prescription;
phosphatidylinositol-3-kinase/protein kinase B /mammalian target of rapamycin （PI3K/Akt/mTOR） signaling pathway;
glycolysis;
drug resistance
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(4):60-69
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism by which Shenqi Yiliu prescription reverses cisplatin resistance in ovarian cancer cells by regulating the phosphatidylinositol-3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway-mediated glycolysis. MethodsThe human ovarian cancer A2780 cell line was intervened with progressively increasing doses of cisplatin （1 g·L-1） to establish the cisplatin-resistant cell line A2780cisR， and the cell sensitivity to cisplatin was examined by the cell counting kit-8 （CCK-8） assay. High， medium， and low （39.9， 19.95， 9.98 g·kg-1） doses of Shenqi Yiliu prescription-containing sera were used to treat A2780cisR cells for 48 h. Glucose consumption and lactate production were measured by the cuvette assay. Enzyme-linked immunosorbent assay （ELISA） was employed to determine the activities of glucose transporter （GLUT）， phosphofructokinase （PFK）， and pyruvate kinase （PK）. Terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL） staining was used to detect apoptosis. Western blot was employed to quantify the protein levels of phosphorylated （p）-PI3K， p-Akt， p-mTOR， hexokinase 2 （HK2）， pyruvate kinase M2 （PKM2）， B-cell lymphoblastoma-2 （Bcl-2）， Bcl-2-associated X-protein （Bax）， and B-lymphoblastoma-2 gene-related promoter （Bad）. Real-time PCR was conducted to determine the mRNA levels of HK2， PKM2， Bax， Bcl-2， and Bad. ResultsThe median inhibitory concentration （IC50） of cisplatin on A2780cisR cells was nearly 3 times that on A2780P cells. Compared with A2780P cells， A2780cisR cells showed increased glucose consumption， lactate production， GLUT， PFK， and PK activities， and mRNA and protein levels of p-PI3K， Akt， p-mTOR， HK2， PKM2， Bax （P<0.05）， and decreased apoptosis rate and Bcl-2 expression （P<0.05）. Compared with A2780cisR cells， medium- and high-dose Shenqi Yiliu prescription reduced the glucose consumption， lactate production， GLUT， PFK， and PK activities， and mRNA and protein levels of p-PI3K， Akt， p-mTOR， HK2， PKM2， Bax， and Bad （P<0.05）， while increasing the apoptosis rate and Bcl-2 expression （P<0.05）. ConclusionShenqi Yiliu prescription can inhibit glycolysis mediated by the PI3K/Akt/mTOR pathway to promote apoptosis， thereby reversing cisplatin resistance in ovarian cancer cells.
