Androgen deprivation-induced senescence

Androgen deprivation-induced senescence (or ADIS) refers to the induction of cellular senescence as a result of androgen deprivation therapy.[1][2][3][4][5] ADIS is observed in prostate cancer cells that are dependent on androgens for cell proliferation. Androgen withdrawal induces cells to undergo cellular senescence by up-regulating intracellular reactive oxygen species (ROS) that cause DNA damage. ADIS is maintained through the up-regulation of the cell cycle regulator p16ink4a.

References

  1. Pernicová, Z; Slabáková, E; Kharaishvili, G; Bouchal, J; Král, M; Kunická, Z; Machala, M; Kozubík, A; Souček, K (June 2011). "Androgen depletion induces senescence in prostate cancer cells through down-regulation of Skp2". Neoplasia. 13 (6): 526–36. PMC 3114246Freely accessible. PMID 21677876.
  2. Ewald, JA; Desotelle, JA; Church, DR; Yang, B; Huang, W; Laurila, TA; Jarrard, DF (March 2013). "Androgen deprivation induces senescence characteristics in prostate cancer cells in vitro and in vivo". The Prostate. 73 (4): 337–45. doi:10.1002/pros.22571. PMID 22911222.
  3. Burton, Dominick G. A.; Giribaldi, Maria G.; Munoz, Anisleidys; Halvorsen, Katherine; Patel, Asmita; Jorda, Merce; Perez-Stable, Carlos; Rai, Priyamvada; Agoulnik, Irina U. (27 June 2013). Agoulnik, Irina U, ed. "Androgen Deprivation-Induced Senescence Promotes Outgrowth of Androgen-Refractory Prostate Cancer Cells". PLoS ONE. 8 (6): e68003. doi:10.1371/journal.pone.0068003. PMC 3695935Freely accessible. PMID 23840802.
  4. Barakat et al (2015). CCAAT/Enhancer binding protein β controls androgen-deprivation-induced senescence in prostate cancer cells Oncogene {{doi:10.1038/onc.2015.41}}
  5. Kawata, Hirotoshi; Kamiakito, Tomoko; Nakaya, Takeo; Komatsubara, Maiko; Komatsu, Kenji; Morita, Tatsuo; Nagao, Yasumitsu; Tanaka, Akira. "Stimulation of cellular senescent processes, including secretory phenotypes and anti-oxidant responses, after androgen deprivation therapy in human prostate cancer". The Journal of Steroid Biochemistry and Molecular Biology. doi:10.1016/j.jsbmb.2016.06.007.


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