Table 2 Autophagy as a regulator of therapy response of prostate cancer cells

Pro-survival

Docetaxel resistance

FOXM1 induces chemoresistance of prostate cancer cells in vivo and in vitro.

Increased autophagy flux and formation of autophagosomes.

Targeting the AMPK-MTOR axis in favor of autophagy induction.

FOXM1 enhances docetaxel sensitivity of prostate cancer cells.

[217]

Pro-survival

AKT inhibitor resistance

AKT inhibitor AZD5363 induces both cell cycle arrest and autophagy, but no significant apoptosis induction observed.

Autophagy inhibition using lysosomotropic agents leads to higher potential of AKT inhibitors in prostate cancer therapy.

[218]

Pro-survival

Cisplatin resistance

Silencing CFTR inhibits autophagy to promote cisplatin sensitivity of prostate cancer cells.

Stimulation of AKT-MTOR signaling occurs after CFTR downregulation.

[219]

Pro-death

Radiotherapy

Decreased colony formation using a combination of gamma irradiation and photodynamic therapy.

Decreasing cell viability.

Inducing necrosis and autophagy, but not apoptosis.

[220]

Pro-death

Radiotherapy

MTOR inhibition leads to autophagy induction and enhanced sensitivity to radiotherapy.

Apoptosis blockade or caspase inhibition potentiates autophagy induction.

[221]

Pro-death

Radiotherapy

FBP1 downregulation results in autophagy stimulation via the AMPK-MTOR axis.

Removing protective autophagy and enhancing radio-sensitivity.

[222]

Pro-death

Paclitaxel sensitivity

Autophagy induction upon exposing prostate cancer cells to ultrasound (sonodynamic therapy).

Inducing ER stress.

Inhibiting the PI3K-AKT-MTOR axis via ER stress and subsequent autophagy stimulation.

[223]

Pro-death

Immunotherapy

ESK981 diminished viability of cancer cells.

Inducing cell cycle arrest at G2/M phase.

Inhibition of autophagy flux by ESK981.

[224]