Nuclear receptors in cell life and death
- PMID: 11701345
- DOI: 10.1016/s1043-2760(01)00502-1
Nuclear receptors in cell life and death
Abstract
The balance between cell proliferation and programmed cell death (apoptosis) determines body patterns during animal development and controls compartment sizes, tissue architecture and remodeling. The removal of primordial structures by apoptosis allows the organism to develop sex specifically and to adapt for novel functions at later stages; apoptosis also limits the size of evolving structures. It is a ubiquitous function that is essential for all cells. Although inappropriate regulation or execution of apoptosis leads to disease, such as cancer, there is now evidence for its great therapeutic potential. This would be particularly true if apoptosis could be targeted at defined cell compartments, rather than acting ubiquitously like chemotherapy. Here, we discuss the potential of nuclear receptor ligands, many of which act through their cognate receptors in defined body compartments as modulators of cell life and death, with special emphasis on the molecular pathways by which these receptors affect cell-cycle progression, survival and apoptosis.
Similar articles
-
Principles for modulation of the nuclear receptor superfamily.Nat Rev Drug Discov. 2004 Nov;3(11):950-64. doi: 10.1038/nrd1551. Nat Rev Drug Discov. 2004. PMID: 15520817 Review.
-
Cell survival, cell death and cell cycle pathways are interconnected: implications for cancer therapy.Drug Resist Updat. 2007 Feb-Apr;10(1-2):13-29. doi: 10.1016/j.drup.2007.01.003. Epub 2007 Feb 14. Drug Resist Updat. 2007. PMID: 17303468 Review.
-
Hormone nuclear receptors and their ligands: role in programmed cell death (review).Endocr Regul. 2002 Mar;36(1):37-60. Endocr Regul. 2002. PMID: 11971750 Review.
-
Reversible nuclear translocation of glyceraldehyde-3-phosphate dehydrogenase upon serum depletion.Eur J Cell Biol. 2001 Jun;80(6):419-27. doi: 10.1078/0171-9335-00174. Eur J Cell Biol. 2001. PMID: 11484933
-
Get a ligand, get a life: integrins, signaling and cell survival.J Cell Sci. 2002 Oct 1;115(Pt 19):3729-38. doi: 10.1242/jcs.00071. J Cell Sci. 2002. PMID: 12235283 Review.
Cited by
-
Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer.Int J Clin Exp Pathol. 2013 Aug 15;6(9):1817-25. eCollection 2013. Int J Clin Exp Pathol. 2013. PMID: 24040446 Free PMC article.
-
Retinoid- and sodium-butyrate-induced decrease in heat shock protein 70 membrane-positive tumor cells is associated with reduced sensitivity to natural killer cell lysis, growth delay, and altered growth morphology.Cell Stress Chaperones. 2005 Summer;10(2):136-46. doi: 10.1379/csc-88r1.1. Cell Stress Chaperones. 2005. PMID: 16038410 Free PMC article.
-
iNR-Drug: predicting the interaction of drugs with nuclear receptors in cellular networking.Int J Mol Sci. 2014 Mar 19;15(3):4915-37. doi: 10.3390/ijms15034915. Int J Mol Sci. 2014. PMID: 24651462 Free PMC article.
-
Apoptosis and molecular targeting therapy in cancer.Biomed Res Int. 2014;2014:150845. doi: 10.1155/2014/150845. Epub 2014 Jun 12. Biomed Res Int. 2014. Retraction in: Biomed Res Int. 2020 Aug 28;2020:2451249. doi: 10.1155/2020/2451249. PMID: 25013758 Free PMC article. Retracted. Review.
-
Antiproliferative effect of 13-cis-retinoic acid is associated with granulocyte differentiation and decrease in cyclin B1 and Bcl-2 protein levels in G0/G1 arrested HL-60 cells.Pathol Oncol Res. 2010 Sep;16(3):393-401. doi: 10.1007/s12253-009-9241-2. Epub 2010 Jan 19. Pathol Oncol Res. 2010. PMID: 20084480
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources