| Simvastatin and Fluvastatin |
0–10 μM (In vitro)
|
|
Inhibit cell proliferation
and promote apoptosis |
Downregulate the phosphorylation
of AKT/FOXO1 |
(31) |
| Simvastatin |
0–50 μM (In vitro)
|
Irinotecan |
Combined therapy suppresses
tumor growth and induces apoptosis |
Inhibit MCL-1 |
(32) |
| 2 mg/kg (In vivo)
|
|
Suppress tumor
growth |
Inhibit Akt
and reduce PSA expression |
(33) |
| 0–100
μM (In vitro)
|
| Atorvastatin |
0–50 μM (In vitro)
|
Irradiation |
Improves the radiosensitivity
of hypoxia-induced PCA cells |
Decreased expression of
hypoxia-inducible factor (HIF-1α) |
(34) |
| 0–5 μM (In vitro)
|
Caffeine |
Combined therapy inhibits
proliferation and increases apoptosis |
Decreased p-Akt, p-Erk1/2, Bcl-2, and survivin levels |
(35) |
| 5 mg/kg
or10 mg/kg (In-vivo)
|
Celecoxib |
Combination suppresses tumor
growth and progression inhibition in SCID mice and Lymph node carcinoma
of the prostate (LNCaP) PCA |
Akt, Erk1/2, and NF-κB activation |
(36), (37) |
| 0–10 μM (In vitro)
|
It also induces autophagy
(PCA-3 cells) |
Induction
of light chain
3 (LC3) transcription |
| Atorvastatin, Mevastatin,
Simvastatin, and Rosuvastatin |
0–10 μM (In vitro)
|
|
Lower migration and colonies
(PCA-3 cells) |
Inhibit
GGPP synthesis |
(38) |
| Lovastatin and Simvastatin |
0–2 μM (In vitro)
|
|
Induction of apoptosis induction
and cell cycle arrest in the G1 phase |
RhoA inactivation |
(19) |
