Related Experiment Video
Updated: Aug 27, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Luteolin Reduces Aqueous Extract PM2.5-induced Metastatic Activity in H460 Lung Cancer Cells
Hui-Wen Lin1,2, Ting-Jing Shen3, Nae-Cherng Yang4
1Department of Optometry, Asia University, Taichung, Taiwan.
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.
Insights
Fine particulate matter (PM2.5) promotes lung cancer. This study shows luteolin blocks PM2.5-induced cancer progression by inhibiting the EGFR-PI3K-AKT pathway, reducing cell migration and metastasis.
Area of Science:
- Environmental Health
- Cancer Biology
- Pharmacology
Background:
- Fine particulate matter (PM2.5) is a known carcinogen, significantly contributing to lung cancer development.
- PM2.5 exposure promotes tumor cell migration and invasion, exacerbating cancer progression.
- Flavonoids, like luteolin, possess antiangiogenic properties and are investigated for their potential anti-cancer effects.
Purpose of the Study:
- To investigate the efficacy of luteolin in inhibiting PM2.5-induced lung cancer progression.
- To elucidate the molecular mechanisms by which luteolin affects cancer cell migration and metastasis.
- To determine the role of the epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT) signaling pathway in luteolin's anti-cancer effects.
Main Methods:
- Utilized aqueous extract of PM2.5 and H460 human lung cancer cells.
- Assessed the effects of luteolin on cell migration and invasion.
- Measured the expression levels of pro-metastatic factors, including matrix metalloproteinase-2 (MMP-2) and intercellular adhesion molecule-1 (ICAM-1).
- Investigated the involvement of the EGFR-PI3K-AKT signaling cascade.
Main Results:
- Luteolin significantly reduced cell migration in PM2.5-exposed H460 cells.
- Luteolin decreased the expression of MMP-2 and ICAM-1, key factors in metastasis.
- Luteolin treatment inhibited the PM2.5-induced activation of the EGFR-PI3K-AKT signaling pathway.
- The inhibitory effects of luteolin on MMP-2 and ICAM-1 were dependent on the EGFR-PI3K-AKT pathway.
Conclusions:
- Luteolin demonstrates potent anti-cancer properties against PM2.5-induced lung cancer progression.
- Luteolin effectively inhibits tumor cell migration and metastasis by targeting the EGFR-PI3K-AKT pathway.
- These findings highlight luteolin as a potential therapeutic agent for mitigating the adverse effects of PM2.5 exposure on lung cancer.
More Related Videos
07:39The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
08:47Improved Visualization of Lung Metastases at Single Cell Resolution in Mice by Combined In-situ Perfusion of Lung Tissue and X-Gal Staining of lacZ-Tagged Tumor Cells
Published on: August 21, 2012