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Table 1 Treatments that induce cellular senescence in PCa with indicated mechanisms

From: Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer

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]