title: Protector turns predator: Autophagic death via selective degradation of KRAS.
abstract: Therapy-induced autophagy is recognized as a critical determinant of treatment outcome in cancer patients, primarily as a factor underlying drug resistance. However, recent investigations point toward a context-dependent, death-inducing role for autophagy, the mechanism of which remains largely unknown. Our recent study provides evidence that autophagy can directly mediate cell killing in multiple tumor cell types by facilitating degradation of KRAS/K-Ras, a key survival protein. These findings have broad implications for strategies employing autophagy modulation to target tumor cells.
authors.affiliation: Department of Pathology; University of Alabama at Birmingham; Birmingham, AL USA; Department of Cell Biology; University of Alabama at Birmingham; Birmingham, AL USA.
authors.forename: Latika
authors.initials: L
authors.lastname: Kohli
authors.forename: Niroop
authors.initials: N
authors.lastname: Kaza
authors.forename: Steven L
authors.initials: SL
authors.lastname: Carroll
authors.forename: Kevin A
authors.initials: KA
authors.lastname: Roth
mesh_terms: D001343:Autophagy / Q000187:drug effects; D019610:Cytoprotection / Q000187:drug effects; D020935:MAP Kinase Signaling System / Q000187:drug effects; D011493:Protein Kinase C / Q000378:metabolism; D059748:Proteolysis / Q000187:drug effects; D016283:Proto-Oncogene Proteins p21(ras) / Q000378:metabolism*; D013629:Tamoxifen / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D013629:Tamoxifen; C016601:afimoxifene; D011493:Protein Kinase C; D016283:Proto-Oncogene Proteins p21(ras)
keywords: EGFR; KRAS; PRKC; autophagy; tamoxifen; tumor cells