Ectopic ERK expression induces phenotypic conversion of C10 cells and alters DNA methyltransferase expression.

摘要: Many lung carcinogens activate mitogen activated protein kinase (MAPK) pathways and DNA methyltransferases (DNMTs) are under investigation as therapeutic targets for cancer. Our goal is to determine whether C10 type II alveolar epithelial cells a sensitive model investigate ERK-dependent transformation DNMT expression patterns in experimental Ectopic of an extracellular signal regulated (ERK)-green fluorescent (ERK1-GFP) induces acquisition growth soft agar that selectively associated with latent effects on the methyl transferases (DNMT1 3b), xeroderma pigmentosum complementation group A (XPA), DNA-dependent catalytic subunit (DNA-PKcs), increased phosphatase activity enhanced sensitivity 5-azacytidine (5-azaC)-mediated toxicity, relative controls. ERK alone sufficient promote phenotypic conversion altered inhibitor. This may have applications predicting inhibitors.