title: c-Myc oncoprotein: cell cycle-related events and new therapeutic challenges in cancer and cardiovascular diseases.
abstract: Advanced stages of both cancer and atherosclerosis are characterized by a local increase in tissue mass that may be hard to control. This increase in tissue mass can be attributed to oxidation-sensitive modification of cell cycle-related events, including cellular proliferation, differentiation, and apoptosis, which could be secondary to alteration in the activity of tumor suppressor gene and oncogene products. The oncogene c-Myc has classically been considered to be involved in carcinogenesis and has more recently been implicated in both endothelial dysfunction and atherogenesis as well. Consequently, inhibition of c-Myc-dependent signaling has become a novel therapeutic opportunity and challenge in atherosclerosis and other cardiovascular diseases. Antioxidant strategies, RNA synthesis inhibitors such as mithramycin, and gene therapeutic approaches with antisense oligonucleotides against c-Myc are some of the promising strategies. In general, the increased biologic understanding of the participation of cell cycle events and targeting these events may enable to attenuate or prevent some of the complications of vascular and neoplastic diseases.
authors.affiliation: Department of Pharmacological Sciences, University of Salerno, Salerno, Italy.
authors.forename: Filomena
authors.initials: F
authors.lastname: de Nigris
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Sica
authors.forename: Joerg
authors.initials: J
authors.lastname: Herrmann
authors.forename: Gianluigi
authors.initials: G
authors.lastname: Condorelli
authors.forename: Alejandro R
authors.initials: AR
authors.lastname: Chade
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Tajana
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.forename: Claudio
authors.initials: C
authors.lastname: Napoli
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000378:metabolism* / Q000503:physiopathology; D002453:Cell Cycle; D018797:Cell Cycle Proteins; D002454:Cell Differentiation / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D004268:DNA-Binding Proteins; D050684:E2F Transcription Factors; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology; D015316:Genetic Therapy; D006801:Humans; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000378:metabolism*; D009369:Neoplasms / Q000378:metabolism* / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D017239:Paclitaxel / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D016271:Proto-Oncogene Proteins c-myc / Q000187:drug effects / Q000378:metabolism*; D011817:Rabbits; D020123:Sirolimus / Q000494:pharmacology; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D000975:Antioxidants; D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D050684:E2F Transcription Factors; D005419:Flavonoids; D010880:Piperidines; D016271:Proto-Oncogene Proteins c-myc; D014157:Transcription Factors; D009569:Nitric Oxide; C077990:alvocidib; D017239:Paclitaxel; D020123:Sirolimus