Hackler, Patrick C.Reuss, SarahKonger, Raymond L.Travers, Jeffrey B.Sahu, Ravi P.2025-04-022025-04-022014-06-19Hackler PC, Reuss S, Konger RL, Travers JB, Sahu RP. Systemic Platelet-activating Factor Receptor Activation Augments Experimental Lung Tumor Growth and Metastasis. Cancer Growth Metastasis. 2014;7:27-32. Published 2014 Jun 19. doi:10.4137/CGM.S14501https://hdl.handle.net/1805/46757Pro-oxidative stressors including cigarette smoke (CS) generate novel lipids with platelet-activated factor-receptor (PAF-R) agonistic activity mediate systemic immunosuppression, one of the most recognized events in promoting carcinogenesis. Our previous studies have established that these oxidized-PAF-R-agonists augment murine B16F10 melanoma tumor growth in a PAF-R-dependent manner because of its effects on host immunity. As CS generates PAF-R agonists, the current studies sought to determine the impact of PAF-R agonists on lung cancer growth and metastasis. Using the murine Lewis Lung Carcinoma (LLC1) model, we demonstrate that treatment of C57BL/6 mice with a PAF-R agonist augments tumor growth and lung metastasis in a PAF-R-dependent manner as these findings were not seen in PAF-R-deficient mice. Importantly, this effect was because of host rather than tumor cells PAF-R dependent as LLC1 cells do not express functional PAF-R. These findings indicate that experimental lung cancer progression can be modulated by the PAF system.en-USAttribution-NonCommercial 4.0 InternationalLung cancer growth and metastasisPlatelet-activating factor-receptorPro-oxidative stressorsSystemic immunosuppressionArticle