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

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...

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Published inInternational journal of medical sciences Vol. 19; no. 10; pp. 1502 - 1509
Main Authors Lin, Hui-Wen, Shen, Ting-Jing, Yang, Nae-Cherng, Wang, Meilin, Hsieh, Wen-Che, Chuang, Chen-Ju, Lai, Chane-Yu, Chang, Yuan-Yen
Format Journal Article
LanguageEnglish
Published Wyoming Ivyspring International Publisher Pty Ltd 01.01.2022
Ivyspring International Publisher
Subjects
Antibodies
Cell adhesion & migration
Cell culture
Cell cycle
Cytotoxicity
Flavonoids
Kinases
Lung cancer
Metastasis
Mortality
Proteins
Research Paper
Tumor necrosis factor-TNF
Wound healing
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Summary: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.
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These authors contributed equally to this work.
Competing Interests: The authors have declared that no competing interest exists.
ISSN:1449-1907
1449-1907
DOI:10.7150/ijms.73947