Cellular senescence and cancer treatment
- PMID: 17027159
- DOI: 10.1016/j.bbcan.2006.08.005
Cellular senescence and cancer treatment
Abstract
Cellular senescence, an irreversible cell-cycle arrest, reflects a safeguard program that limits the proliferative capacity of the cell exposed to endogenous or exogenous stress signals. A number of recent studies have clarified that an acutely inducible form of cellular senescence may act in response to oncogenic activation as a natural barrier to interrupt tumorigenesis at a premalignant level. Paralleling the increasing insights into premature senescence as a tumor suppressor mechanism, a growing line of evidence identifies cellular senescence as a critical effector program in response to DNA damaging chemotherapeutic agents. This review discusses molecular pathways to stress-induced senescence, the interference of a terminal arrest condition with clinical outcome, and the critical overlap between premature senescence and apoptosis as both tumor suppressive and drug-responsive cellular programs.
Similar articles
-
DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis.J Zhejiang Univ Sci B. 2007 Jun;8(6):377-97. doi: 10.1631/jzus.2007.B0377. J Zhejiang Univ Sci B. 2007. PMID: 17565509 Free PMC article. Review.
-
Oncogene- and tumor suppressor gene-mediated suppression of cellular senescence.Semin Cancer Biol. 2011 Dec;21(6):367-76. doi: 10.1016/j.semcancer.2011.10.005. Epub 2011 Oct 24. Semin Cancer Biol. 2011. PMID: 22037160 Review.
-
DNA-damaging imidazoacridinone C-1311 induces autophagy followed by irreversible growth arrest and senescence in human lung cancer cells.J Pharmacol Exp Ther. 2013 Sep;346(3):393-405. doi: 10.1124/jpet.113.203851. Epub 2013 Jul 3. J Pharmacol Exp Ther. 2013. PMID: 23823138
-
Accelerated senescence: an emerging role in tumor cell response to chemotherapy and radiation.Biochem Pharmacol. 2008 Oct 15;76(8):947-57. doi: 10.1016/j.bcp.2008.06.024. Epub 2008 Jul 9. Biochem Pharmacol. 2008. PMID: 18657518
-
Irreversible cellular senescence induced by prolonged exposure to H2O2 involves DNA-damage-and-repair genes and telomere shortening.Int J Biochem Cell Biol. 2005 Jul;37(7):1407-20. doi: 10.1016/j.biocel.2005.01.010. Int J Biochem Cell Biol. 2005. PMID: 15833273
Cited by
-
Different Approaches for the Profiling of Cancer Pathway-Related Genes in Glioblastoma Cells.Int J Mol Sci. 2022 Sep 17;23(18):10883. doi: 10.3390/ijms231810883. Int J Mol Sci. 2022. PMID: 36142793 Free PMC article.
-
Cancer and radiation therapy: current advances and future directions.Int J Med Sci. 2012;9(3):193-9. doi: 10.7150/ijms.3635. Epub 2012 Feb 27. Int J Med Sci. 2012. PMID: 22408567 Free PMC article. Review.
-
Activation of p53 with Nutlin-3a radiosensitizes lung cancer cells via enhancing radiation-induced premature senescence.Lung Cancer. 2013 Aug;81(2):167-73. doi: 10.1016/j.lungcan.2013.04.017. Epub 2013 May 16. Lung Cancer. 2013. PMID: 23683497 Free PMC article.
-
Combination therapy of cisplatin and resveratrol to induce cellular aging in gastric cancer cells: Focusing on oxidative stress, and cell cycle arrest.Front Pharmacol. 2023 Jan 4;13:1068863. doi: 10.3389/fphar.2022.1068863. eCollection 2022. Front Pharmacol. 2023. PMID: 36686661 Free PMC article.
-
BMP4-Smad signaling pathway mediates adriamycin-induced premature senescence in lung cancer cells.J Biol Chem. 2009 May 1;284(18):12153-64. doi: 10.1074/jbc.M807930200. Epub 2009 Mar 6. J Biol Chem. 2009. PMID: 19269967 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases
