title: Molecular targets for selenium in cancer prevention.
abstract: Mounting evidence reveals that selenium is a dietary constituent with anticarcinogenic and antitumorigenic properties. Various forms of selenium appear to be effective in bringing about these effects, although preclinical studies suggest that differences may arise as the quantity provided is reduced. The literature also documents the greater sensitivity of neoplastic cells to selenium than their nonneoplastic counterparts. Unfortunately, the minimal amount needed to bring about a positive effect in humans remains elusive. If there is a positive response to exaggerated intakes, it will likely be dependent on many factors, including the consumption of other dietary constituents, as well as variation in a host of genetic pathways involved with cancer. Although the biological basis of the reduction in cancer risk ascribed to selenium remains to be established, its consistency in retarding various experimentally induced tumors and suppressing the growth of various types of neoplasms in vitro and in vivo suggests that several mechanisms are involved. Depressed carcinogen bioactivation, reduced cell proliferation, and increased apoptosis raise the possibility that selenium works at a number of specific molecular targets involved with the cancer process. This review will focus on molecular targets involved with cell proliferation and apoptosis as possible mechanisms by which selenium might alter the cancer process.
authors.affiliation: Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville, MD 20892, USA.
authors.forename: Y S
authors.initials: YS
authors.lastname: Kim
authors.forename: J
authors.initials: J
authors.lastname: Milner
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000008:administration & dosage* / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000008:administration & dosage* / Q000494:pharmacology; D000975:Antioxidants / Q000008:administration & dosage* / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D042846:CDC2-CDC28 Kinases; D002455:Cell Division / Q000187:drug effects; D051357:Cyclin-Dependent Kinase 2; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008084:Lipoxygenase / Q000187:drug effects; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D009369:Neoplasms / Q000517:prevention & control*; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors; D011506:Proteins / Q000037:antagonists & inhibitors; D012643:Selenium / Q000008:administration & dosage* / Q000737:chemistry / Q000494:pharmacology; D018808:Transcription Factor AP-1 / Q000037:antagonists & inhibitors; D000097642:GADD45 Proteins
chemical_list: D016588:Anticarcinogenic Agents; D000970:Antineoplastic Agents; D000975:Antioxidants; D042846:CDC2-CDC28 Kinases; D051357:Cyclin-Dependent Kinase 2; D018844:Cyclin-Dependent Kinases; D047908:Intracellular Signaling Peptides and Proteins; D008084:Lipoxygenase; D016328:NF-kappa B; D017346:Protein Serine-Threonine Kinases; D011506:Proteins; D012643:Selenium; D018808:Transcription Factor AP-1; D000097642:GADD45 Proteins; C495894:CDK2 protein, human