Molecular Mechanism of Gypenoside L in Anti-Ovarian Cancer by Affecting GCK-Mediated Glycolytic Pathway
10.13422/j.cnki.syfjx.20250319
- VernacularTitle:绞股蓝皂苷L影响GCK介导的糖酵解途径抗卵巢癌分子机制
- Author:
Yuanguang DONG
1
;
Nan SONG
1
;
Ying YANG
1
;
Jingxuan ZHU
1
;
Jiaxin WANG
1
;
Mingdian YUAN
2
;
Yingying SUN
1
Author Information
1. Liaoning University of Traditional Chinese Medicine（TCM）， Shenyang 110847，China
2. Liaoning Provincial Hospital of TCM， Shenyang 110033，China
- Publication Type:Journal Article
- Keywords:
ovarian cancer;
gypenoside L;
glucokinase （GCK）;
glycolysis;
cell proliferation
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(11):118-124
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the molecular mechanism of gypenoside L （Gyp-L） in the treatment of ovarian cancer （OC） by taking the glycolytic pathway of OC as the key point. MethodsThe proliferation activity of OVCAR3 cells was measured by the cell counting kit-8 （CCK-8） assay to determine the appropriate intervention concentration for subsequent experiments. The cell clone formation assay and the scratch healing assay were employed to assess the proliferation and migration capabilities of OVCAR3 cells. OVCAR3 cells were divided into a blank group， a Gyp-L-L group （low concentration of Gyp-L， 50 µmol·L-1）， a Gyp-L-H group （high concentration of Gyp-L， 100 µmol·L-1）， and a cisplatin （15 µmol·L-1） group. The glucose consumption in OC cells was determined using a kit， and the expression levels of related mRNAs in OVCAR3 cells were detected by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The expressions of related proteins were detected by Wes automatic Western blot quantitative analysis. ResultsValidated by the cell scratch assay， the scratch healing rate of OVCAR3 cells was decreased after Gyp-L intervention， reflecting that Gyp-L could significantly inhibit the migration of OVCAR3 cells （P<0.05）. According to the clone formation assay， the cell colony formation ability of the Gyp-L-L group， Gyp-L-H group， and cisplatin group was significantly lower than that of the control group （P<0.05）. In OVCAR3 cells， compared with those in the control group， the levels of glucose consumption and lactate generation in the Gyp-L-L group and Gyp-L-H group were significantly reduced （P<0.05）， indicating that Gyp-L could effectively inhibit the glycolysis level of OC cells. Meanwhile， Gyp-L could suppress the expression levels of glucokinase （GCK）， phosphofructokinase liver （PFKL）， signal transducer and activator of transcription 3 （STAT3）， lactate dehydrogenase D （LDHD）， phosphoglycerate mutase 1 （PGAM1）， mRNAs， and proteins related to the glycolytic pathway in OC cells. ConclusionGyp-L may inhibit the occurrence and development of OC by influencing the GCK-mediated glycolytic pathway.
