Ginkgolic acid suppresses the invasion of HepG2 cells via downregulation of HGF/c‑Met signaling.
Animals
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Cell Survival
/ drug effects
Down-Regulation
Epithelial-Mesenchymal Transition
/ drug effects
Gene Expression Regulation, Neoplastic
/ drug effects
Hep G2 Cells
Hepatocyte Growth Factor
/ metabolism
Humans
Liver Neoplasms
/ drug therapy
Mice
Neoplasm Invasiveness
Phosphorylation
/ drug effects
Proto-Oncogene Proteins c-met
/ metabolism
Salicylates
/ administration & dosage
Signal Transduction
/ drug effects
Xenograft Model Antitumor Assays
Journal
Oncology reports
ISSN: 1791-2431
Titre abrégé: Oncol Rep
Pays: Greece
ID NLM: 9422756
Informations de publication
Date de publication:
Jan 2019
Jan 2019
Historique:
received:
13
04
2018
accepted:
21
09
2018
pubmed:
16
10
2018
medline:
23
1
2019
entrez:
16
10
2018
Statut:
ppublish
Résumé
Liver cancer is one of the most devastating types of cancer worldwide. Despite years of improvements in treatment, the prognosis of patients with this type of malignancy remains poor due to frequent recurrence and metastasis after surgical resection. Ginkgolic acid (GA) is a botanical drug extracted from the seed coat of Ginkgo biloba L. that possesses a wide range of bioactive properties. However, to the best of our knowledge, whether GA can inhibit the invasion of liver cancer cells and the underlying mechanisms remains unknown. The aim of the present study was to investigate the effects of GA on the migration and invasion abilities of liver cancer cells and the underlying molecular mechanism. The results revealed that GA suppressed the migration and invasion abilities of HepG2 cells. In addition, GA treatment inhibited the expression of invasion‑related molecules (MMP‑2 and MMP‑9) and prevented the epithelial‑mesenchymal transition (EMT) of HepG2 cells. Further experiments revealed that GA‑reduced hepatocyte growth factor (HGF) production and suppressed c‑Met phosphorylation may be the underlying mechanisms. Exogenous recombinant HGF supplementation improved the cell invasion ability impaired by GA. Moreover, the in vivo experiment revealed that GA inhibited the tumor growth of liver cancer and prevented EMT. Collectively, these data indicated that GA effectively suppressed the invasion and EMT of HepG2 cells via downregulation of HGF/c‑Met signaling, thus GA may serve as a novel chemotherapeutic agent for the treatment of HCC.
Identifiants
pubmed: 30320342
doi: 10.3892/or.2018.6786
doi:
Substances chimiques
HGF protein, human
0
Salicylates
0
ginkgolic acid
22910-60-7
Hepatocyte Growth Factor
67256-21-7
MET protein, human
EC 2.7.10.1
Proto-Oncogene Proteins c-met
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM