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Table 1 Role of autophagy in proliferation and survival of prostate cancer cells

From: Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

In vitro/In vivo

Cell line/Animal model

Effect on proliferation and survival

Remarks

Refs

In vivo

DU145 cells

Enhancement

PAK1 undergoes upregulation in prostate cancer cells and is necessary for cancer progression.

Regulation of PAK1 by MTOR.

Activation of MTOR promotes expression level of PAK1 and BECN1, increasing tumor growth via autophagy activation.

[108]

In vivo

In vivo

PC3, LNCaP and DU145 cells

Animal models

Enhancement

Inhibiting Warburg effect and simultaneous suppression of autophagy using chloroquine significantly diminishes prostate cancer progression.

[109]

In vivo

In vivo

LNCaP, 22Rv1 and HEK293T cell lines

Xenografts

Enhancement

CAMKK2 inhibition is associated with a decrease in prostate cancer growth via autophagy inhibition.

Autophagy inhibition after CAMKK2 knockdown occurs due to AMPK-ULK1 downregulation.

[110]

In vivo

PC3 cells

Enhancement

ER stress induction via sphingosine-1-phosphate by enhancing ROS levels, autophagy induction and subsequent increase in prostate cancer survival.

[111]

In vivo

HEK293T cells

Reduction

EP300/p300-CREBBP/CBP stimulates autophagy in prostate cancer cells, providing autophagic degradation of CTNNB1/β-catenin, and a significant decrease in progression and survival of prostate cancer cells.

[112]

In vivo

LNCaP cells

Reduction

PLCE1/PLCe undergoes upregulation and enhances prostate cancer progression.

PLCE1 enhances prostate cancer survival via AR signaling activation.

PLCE1 depletion is associated with autophagy activation through the AMPK-ULK1 axis, and subsequent degradation of AR signaling to suppress prostate cancer proliferation.

[113]

In vivo

PC3 cells

Reduction

AR signaling inhibits autophagy in promoting prostate cancer growth.

AR silencing is associated with autophagy induction and tumor growth inhibition.

[114]

In vivo

OC3 cells

Reduction

Overexpression of BSG/CD147 in prostate cancer cells.

Silencing BSG increases GFP-LC3 puncta formation and LC3-II expression.

Autophagy induction impairs proliferation and survival of prostate cancer cells.

[115]