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Salvigenin Suppresses Hepatocellular Carcinoma Glycolysis and Chemoresistance Through Inactivating the

Hui Shao1, Jingyan Chen1, Ali Li1

  • 1Department of Infection, Zhejiang Taizhou Hospital Affiliated to Wenzhou Medical University, Linhai City, 317000, Zhejiang Province, China.

Applied Biochemistry and Biotechnology
|May 2, 2023
PubMed

Insights

Salvigenin inhibits hepatocellular carcinoma (HCC) growth by reducing glycolysis and overcoming 5-fluorouracil resistance. This natural compound targets the PI3K/AKT/GSK-3β pathway, offering potential for HCC treatment.

Area of Science:

  • Biochemistry
  • Oncology
  • Pharmacology

Background:

  • Hepatocellular carcinoma (HCC) remains a significant health challenge with limited therapeutic options.
  • Salvigenin, a trimethoxylated flavone from Scutellariae species, shows anti-tumor effects but its role in HCC is understudied.
  • Understanding Salvigenin's mechanism in HCC is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the anti-tumor effects and underlying mechanisms of Salvigenin in hepatocellular carcinoma (HCC).
  • To evaluate Salvigenin's impact on HCC cell proliferation, migration, invasion, glycolysis, and chemoresistance.
  • To elucidate the specific molecular pathways targeted by Salvigenin in HCC.

Main Methods:

  • In vitro studies involving dose-dependent treatment of HCC cells with Salvigenin.
  • Assays to measure cell viability, colony formation, migration, invasion, apoptosis, glucose uptake, and lactate production.
  • Network pharmacological analysis and Western blotting to identify and validate targeted pathways (PI3K/AKT/GSK-3β).
  • In vivo studies using nude mice to assess Salvigenin's efficacy on tumor growth and apoptosis.

Main Results:

  • Salvigenin significantly inhibited HCC cell proliferation, migration, and invasion in a dose-dependent manner.
  • It weakened aerobic glycolysis by reducing glucose uptake and lactate production, suppressing key glycolytic enzymes.
  • Salvigenin enhanced sensitivity to 5-fluorouracil (5-FU) and reduced chemoresistance in HCC cells.
  • Network analysis and experimental validation confirmed Salvigenin's inhibition of the PI3K/AKT/GSK-3β pathway.
  • In vivo, Salvigenin suppressed tumor growth and promoted apoptosis in HCC xenografts.

Conclusions:

  • Salvigenin exhibits potent anti-cancer properties against HCC by targeting aerobic glycolysis and chemoresistance.
  • The mechanism involves the downregulation of the PI3K/AKT/GSK-3β signaling pathway.
  • Salvigenin demonstrates potential as a therapeutic agent for HCC, possibly in combination with chemotherapy.
Keywords:
ApoptosisChemoresistanceGlycolysisHepatocellular carcinomaPI3KSalvigenin

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