Luteolin Reduces Aqueous Extract PM2.5-induced Metastatic Activity in H460 Lung Cancer Cells

Int J Med Sci. 2022 Aug 21;19(10):1502-1509. doi: 10.7150/ijms.73947. eCollection 2022.

Abstract

Fine particulate matter (PM2.5) is the critical cause of lung cancer and can further promote tumor cell migration and invasion. This study investigated the effects of luteolin, an antiangiogenic flavonoid agent, on blocking aqueous extract PM2.5-prompted cancer progression. We observed that luteolin reduced cell migration and the expression of pro-metastatic factors pro-matrix metalloproteinase (MMP)-2 and intercellular adhesion molecule (ICAM)-1 in PM2.5-exposed H460 lung cancer cells. Luteolin treatment also reduced the transduction of PM2.5-induced epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) cascade signaling. Furthermore, the reduction of MMP-2 expression and ICAM-1 production by luteolin in PM2.5-stimulated H460 cells is EGFR-PI3K-AKT pathway dependent. These results suggest that luteolin exhibits antitumor progression by inhibiting EGFR-PI3K-AKT pathway.

Keywords: EGFR-PI3K-AKT signalling; PM2.5; lung cancer; luteolin; metastasis.

MeSH terms

  • Cell Line, Tumor
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Lung Neoplasms* / drug therapy
  • Lung Neoplasms* / metabolism
  • Luteolin / pharmacology
  • Luteolin / therapeutic use
  • Matrix Metalloproteinase 2* / genetics
  • Matrix Metalloproteinase 2* / metabolism
  • Matrix Metalloproteinase 9 / metabolism
  • Particulate Matter / toxicity
  • Phosphatidylinositol 3-Kinase
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism

Substances

  • Particulate Matter
  • Intercellular Adhesion Molecule-1
  • Phosphatidylinositol 3-Kinase
  • ErbB Receptors
  • Proto-Oncogene Proteins c-akt
  • Matrix Metalloproteinase 2
  • Matrix Metalloproteinase 9
  • Luteolin