Phosphorylation of FADD by the kinase CK1α promotes KRASG12D-induced lung cancer.

ABSTRACT: Genomic amplification of the gene encoding and phosphorylation of the protein FADD (Fas-associated death domain) is associated with poor clinical outcome in lung cancer and in head and neck cancer. Activating mutations in the guanosine triphosphatase RAS promotes cell proliferation in various cancers. Increased abundance of phosphorylated FADD in patient-derived tumor samples predicts poor clinical outcome. Using immunohistochemistry analysis and in vivo imaging of conditional mouse models of KRAS(G12D)-driven lung cancer, we found that the deletion of the gene encoding FADD suppressed tumor growth, reduced the proliferative index of cells, and decreased the activation of downstream effectors of the RAS-MAPK (mitogen-activated protein kinase) pathway that promote the cell cycle, including

SUBMITTER: Bowman BM 

PROVIDER: S-EPMC4416214 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature