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Effect of curcumin on vascular endothelial growth factor in hypoxic HepG2 cells via the insulin-like growth factor 1

Yihui Chen1, Wei Zhong1, Baohua Chen2

  • 1Department of General Surgery, The 175th Hospital of PLA, Affiliated Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000, P.R. China.

Experimental and Therapeutic Medicine
|March 31, 2018
PubMed

Insights

Curcumin inhibits angiogenesis in liver cancer cells by blocking key signaling pathways. This study explores curcumin's anti-angiogenic effects on HepG2 cells under hypoxia, targeting insulin-like growth factor 1 receptor (IGF-1R).

Area of Science:

  • Hepatocellular carcinoma research
  • Molecular oncology
  • Drug discovery and development

Background:

  • Angiogenesis is crucial for tumor growth, making it a key therapeutic target.
  • Insulin-like growth factor 1 receptor (IGF-1R) signaling promotes tumor progression and angiogenesis.
  • Curcumin, a natural compound, exhibits potential anti-cancer properties, but its anti-angiogenic mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the anti-angiogenic effects of curcumin on HepG2 cells under hypoxic conditions.
  • To elucidate the molecular mechanisms underlying curcumin's action, focusing on the IGF-1R pathway.
  • To assess curcumin's impact on key angiogenesis-related proteins and signaling molecules.

Main Methods:

  • HepG2 cells with IGF-1R knockout were generated using CRISPR/Cas9 technology.
  • Hypoxic conditions were induced using cobalt chloride (CoCl2).
  • Cell viability was assessed using MTT assays, and protein expression (IGF-1R, p-Akt, p-Erk1/2, HIF-1α, VEGF) was analyzed via Western blot.

Main Results:

  • Cobalt chloride induced hypoxia, increasing cell viability reduction and upregulating hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) expression.
  • Curcumin significantly inhibited the expression of phosphorylated-protein kinase B (p-Akt), phosphorylated-extracellular signal-regulated kinases (p-Erk1/2), HIF-1α, and VEGF in hypoxia-induced IGF-1R knockout HepG2 cells.
  • Curcumin demonstrated a dose- and time-dependent inhibitory effect on cell viability under hypoxic conditions.

Conclusions:

  • Curcumin effectively inhibits angiogenesis in HepG2 cells under hypoxic conditions, partly through the IGF-1R pathway.
  • Curcumin suppresses key signaling molecules involved in angiogenesis, including HIF-1α and VEGF.
  • These findings suggest curcumin holds potential as an anti-cancer agent for inhibiting tumor growth by targeting angiogenesis.
Keywords:
HepG2curcuminhypoxiahypoxia inducible factor-1αinsulin-like growth factor 1 receptorknockoutvascular endothelial growth factor

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