Aromatic turmerone regulates the migration and autophagy of cutaneous squamous cell carcinoma cells through the Igf-1/Pi3k/Akt pathway

Pak J Pharm Sci. 2025 Mar-Apr;38(2):381-386.

Abstract

In recent years, the incidence of cutaneous squamous cell carcinoma (CSCC) has been increasing year by year. Due to its characteristics of high recurrence and high invasion, CSCC poses a great potential threat to the prognosis of patients. Aromatic turmerone, an active component of Curcuma longa, has been shown to have anti-tumor, anti-inflammatory and anti-oxidation effects in modern pharmacological research, but its influence on CSCC remains unclear. In this study, we used AT to intervene in human CSCC A431 cell line. The results showed that the growth ability of A431 was significantly inhibited by the intervention of AT. Also, we found that compared to normal A431, the cell invasion number and migration rate of A431 were reduced to (116.00±8.00) and (39.87±4.20) %, respectively, after the intervention of AT. And detecting the inflammatory response in the cells, we found that AT reduced the inflammatory factors and oxidative stress in A431. Meanwhile, aromatic turmerone suppressed the autophagy of A431 and silenced the IGF-1/PI3K/AKT pathway expression, which further reveals the mechanism and pathway of action of aromatic turmerone on CSCC, laying a reliable foundation for the clinical application of aromatic turmerone.

MeSH terms

  • Autophagy* / drug effects
  • Carcinoma, Squamous Cell* / drug therapy
  • Carcinoma, Squamous Cell* / enzymology
  • Carcinoma, Squamous Cell* / metabolism
  • Carcinoma, Squamous Cell* / pathology
  • Cell Line, Tumor
  • Cell Movement* / drug effects
  • Cell Proliferation / drug effects
  • Humans
  • Insulin-Like Growth Factor I* / metabolism
  • Oxidative Stress / drug effects
  • Phosphatidylinositol 3-Kinases* / metabolism
  • Proto-Oncogene Proteins c-akt* / metabolism
  • Sesquiterpenes* / pharmacology
  • Signal Transduction / drug effects
  • Skin Neoplasms* / drug therapy
  • Skin Neoplasms* / enzymology
  • Skin Neoplasms* / metabolism
  • Skin Neoplasms* / pathology

Substances

  • Proto-Oncogene Proteins c-akt
  • Insulin-Like Growth Factor I
  • Phosphatidylinositol 3-Kinases
  • Sesquiterpenes
  • IGF1 protein, human