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] |