GPER介导的大气细颗粒物致肺癌作用研究进展OA

Lung cancer remains the leading cause of cancer-related death worldwide.Fine particulate matter(PM2.5),classified as a group I human carcinogen,has been extensively linked to lung cancer development through epidemiological studies.The G protein-coupled estrogen receptor(GPER)can be activated and induce tumorigenesis by environmental pol-lutants,and it is significantly overexpressed in lung cancer tissues,highlighting its critical role in disease progression.Research indicates that environmental estrogen-like components and metal ions in PM2.5 can activate GPER,thereby regulating down-stream signaling pathways such as mitogen-activated protein kinase/extracellular signal-regulated kinase(MAPK/ERK)and phosphoinositide 3-kinase/protein kinase B(PI3K/AKT).This activation triggers inflammatory responses,oxidative stress,and ferroptosis,ultimately promoting tumor cell proliferation,apoptosis,migration,epithelial-mesenchymal transition,and remodeling of the tumor microenvironment.Collectively,these mechanisms drive the initiation and progression of lung can-cer.In summary,GPER serves as a pivotal molecular hub connecting PM2.5 exposure to lung cancer pathogenesis,presenting a promising therapeutic target.Inhibitors targeting GPER may offer novel strategies for the prevention and treatment of lung cancer.