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. 2022 Dec 15;12:200. doi: 10.1186/s13578-022-00941-0

Table 1.

Treatments that induce cellular senescence in PCa with indicated mechanisms

Therapy/treatment Dose Model system Mechanism References
Chemotherapy
 Docetaxel 5 nM LNCaP Anti-microtubule agent [116]
 Doxorubicin 25 nM DU145/LNCaP Anthracyclines, DNA damage [116]
 Mitoxantrone BPH-1, RWPE-1, and PC3 Anthracyclines, DNA damage, p16INK4a, p21WAF1/CIP1 [32]
 5-azacytidine 0.375 µM/75 µM DU145/LNCaP Antimetabolite, inhibition of DNA methyltransferase [116]
 Diaziquone 10 µM DU145, LNCaP, PC3 DNA alkylation, p27Kip1 [115, 125]
 Bithionol 10 µM DU145, LNCaP unknown [115]
 Dichlorophene 10 µM DU145, LNCaP unknown [115]
 Pyrithione 10 µM DU145, LNCaP Zn2+ ionophore, oxidative stress, ERK [115]
Radiotherapy
 Gamma radiation 2–10 Gy Primary prostate epithelial cells DNA damage response [52]
 Gamma radiation 4 and 10 Gy DU145, LNCaP, 22Rv1 DNA damage response [56, 58]
 X radiation 2, 4 and 8 Gy PC3 P53, p21 WAF1/CIP1, p16INK4a, p15INK4b [55]
AR targeted therapy
 ADT LNCaP, LAPC-4, LuCaP xenograft, PCa patient samples

p27Kip1, C/EBP β,

oxidative stress, p16INK4a

[8, 67, 68]
AR agonist
 Dihydrotestosterone 10 nM

PC3, LNCaP, C4-2

PCa patient samples

p16INK4a, p21WAF1/CIP1, Cyclin D1, pRb, [86, 184]
 Methyltrienolone 1 nM

PC3, LNCaP, C4-2

PCa patient samples

p16INK4a, p21WAF1/CIP1, p27Kip1, Cyclin D1, E2F1, pRb, Src, AKT [86, 90]
AR antagonists
 Bicalutamide 0.5–100 µM LNCaP, CWR22PC p16INK4a, p27Kip1 [68, 92]
 Enzalutamide 10 µM LNCaP, C4-2, LNCaP and C4-2 xenograft p16INK4a [88, 94, 185]
 Darolutamide 10 µM LNCaP, C4-2 p16INK4a [94]
 Atraric acid 1- 30 µM

LNCaP, C4-2 xenograft

PCa patient samples

p16INK4a, pRb, Src, AKT [91, 101]

 20-aminosteroid

(C18)

10 µM LNCaP Unknown [95]
 Anthranilic acid ester (C28) 30 µM LNCaP Unknown [102]