title: Crosstalk between ERK, AKT, and cell survival.
abstract: It is historically well known that signaling by the PI3K-AKT and MEK1/2-ERK1/2 pathways in a cell type-dependent fashion can collaborate to maintain cell viability. (1)(-) (3) Signaling pathways can also crosstalk with each other wherein one pathway can signal to either enhance or suppress signaling by another. (4) Signaling by the ERK1/2 pathway can also stimulate release of growth factors which can feed back onto tumor cells to re-energize signaling pathways. (5) The studies described by Toulany et al. add to this knowledge base by examining the relationship between PI3K-AKT and MEK1/2-ERK1/2 pathway signaling, EGF receptor signaling, K-RAS function, and tumor cell survival. (6.)
authors.affiliation: Department of Biochemistry; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.
authors.forename: Paul
authors.initials: P
authors.lastname: Dent
mesh_terms: D006801:Humans; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D051058:Oncogene Protein v-akt / Q000378:metabolism*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins / Q000378:metabolism*
chemical_list: C117307:KRAS protein, human; D000081082:Phosphoinositide-3 Kinase Inhibitors; D011518:Proto-Oncogene Proteins; D051058:Oncogene Protein v-akt; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins
keywords: EGFR; HNSCC; K-RAS; MAPK/ERK; NSCLC; PI-103; PI3K/Akt; erlotinib