title: Harnessing the tumor suppressor function of FOXO as an alternative therapeutic approach in cancer.
abstract: The promotion of cellular survival, dedifferentiation, and uncontrolled proliferation via the suppression of apoptotic effectors is a fundamental characteristic of tumor cells. As substrates that are negatively regulated by oncogenic signaling cascades driven by AKT, SGK (serum- and glucocorticoid-inducible kinase), IkB kinase (IKK), ERK, and cyclin-dependent kinases (CDK), forkhead box-class O (FOXO) transcription factors have emerged as bona fide tumor suppressors. These transcription factors indeed regulate a variety of cellular responses and themselves are regulated by reversible phosphorylation, acetylation, ubiquitination and miRNAs. This review will discuss our current understanding of mechanisms for FOXO regulation and the potential implications for therapeutically restoring FOXO transcriptional activity.
authors: Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
authors: Amrik
authors: A
authors: Singh
authors: Jessica
authors: J
authors: Plati
authors: Roya
authors: R
authors: Khosravi-Far
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D054337:Cell Dedifferentiation; D049109:Cell Proliferation; D002470:Cell Survival; D051858:Forkhead Transcription Factors / Q000378:metabolism*; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy* / Q000473:pathology; D011499:Protein Processing, Post-Translational
chemical_list: D000970:Antineoplastic Agents; D051858:Forkhead Transcription Factors; D035683:MicroRNAs