Research Paper Volume 13, Issue 3 pp 4357—4369

The hepatic microenvironment promotes lung adenocarcinoma cell proliferation, metastasis, and epithelial–mesenchymal transition via METTL3-mediated N6-methyladenosine modification of YAP1

The hepatic inflammatory microenvironment promoted the proliferation, migration, and invasion of lung adenocarcinoma (LUAD) cells. The IL-6-stimulated inflammatory microenvironment simulated by liver cells (our hepatic inflammatory microenvironment model) significantly promoted the (A) proliferation, (B) migration, and (C) invasiveness of A549 and H1975 LUAD cells and (D) significantly increased the secretion of the primary hepatocyte inflammatory factors CRP, TNFα, and IL-22 (*PP

Figure 1. The hepatic inflammatory microenvironment promoted the proliferation, migration, and invasion of lung adenocarcinoma (LUAD) cells. The IL-6-stimulated inflammatory microenvironment simulated by liver cells (our hepatic inflammatory microenvironment model) significantly promoted the (A) proliferation, (B) migration, and (C) invasiveness of A549 and H1975 LUAD cells and (D) significantly increased the secretion of the primary hepatocyte inflammatory factors CRP, TNFα, and IL-22 (*P<0.05, **P<0.01 versus the control group).