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木樨草素降低了 PM2.5 水提物诱导的 H460 肺癌细胞转移活性。

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

机构信息

Department of Optometry, Asia University, Taichung, Taiwan.

Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40402, Taiwan.

出版信息

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.

摘要

细颗粒物(PM2.5)是肺癌的关键致病因素,并可进一步促进肿瘤细胞迁移和侵袭。本研究探讨了具有抗血管生成作用的类黄酮剂木樨草素对阻断水提 PM2.5 促进癌症进展的影响。我们观察到木樨草素降低了 PM2.5 暴露的 H460 肺癌细胞中的细胞迁移和促转移因子基质金属蛋白酶(MMP)-2 和细胞间黏附分子(ICAM)-1 的表达。木樨草素处理还降低了 PM2.5 诱导的表皮生长因子受体(EGFR)-磷酸肌醇 3-激酶(PI3K)-蛋白激酶 B(AKT)级联信号转导。此外,木樨草素在 PM2.5 刺激的 H460 细胞中对 MMP-2 表达和 ICAM-1 产生的减少依赖于 EGFR-PI3K-AKT 通路。这些结果表明,木樨草素通过抑制 EGFR-PI3K-AKT 通路表现出抗肿瘤进展作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6888/9515691/6857c4e1c02a/ijmsv19p1502g001.jpg

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