GNS561, a clinical-stage PPT1 inhibitor, is efficient against hepatocellular carcinoma via modulation of lysosomal functions
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Published on: July 12, 2018
Sonia Brun1, Eloïne Bestion1,2, Eric Raymond1,3
1Genoscience Pharma, Marseille, France.
Abstract:
Hepatocellular carcinoma is the most frequent primary liver cancer. Macroautophagy/autophagy inhibitors have been extensively studied in cancer but, to date, none has reached efficacy in clinical trials. In this study, we demonstrated that GNS561, a new autophagy inhibitor, whose anticancer activity was previously linked to lysosomal cell death, displayed high liver tropism and potent antitumor activity against a panel of human cancer cell lines and in two hepatocellular carcinoma in vivo models. We showed that due to its lysosomotropic properties, GNS561 could reach and specifically inhibited its enzyme target, PPT1 (palmitoyl-protein thioesterase 1), resulting in lysosomal unbound Zn2+ accumulation, impairment of cathepsin activity, blockage of autophagic flux, altered location of MTOR (mechanistic target of rapamycin kinase), lysosomal membrane permeabilization, caspase activation and cell death. Accordingly, GNS561, for which a global phase 1b clinical trial in liver cancers was just successfully achieved, represents a promising new drug candidate and a hopeful therapeutic strategy in cancer treatment.Abbreviations: ANXA5:annexin A5; ATCC: American type culture collection; BafA1: bafilomycin A1; BSA: bovine serum albumin; CASP3: caspase 3; CASP7: caspase 7; CASP8: caspase 8; CCND1: cyclin D1; CTSB: cathepsin B; CTSD: cathepsin D; CTSL: cathepsin L; CQ: chloroquine; iCCA: intrahepatic cholangiocarcinoma; DEN: diethylnitrosamine; DMEM: Dulbelcco's modified Eagle medium; FBS: fetal bovine serum; FITC: fluorescein isothiocyanate; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HCC: hepatocellular carcinoma; HCQ: hydroxychloroquine; HDSF: hexadecylsulfonylfluoride; IC50: mean half-maximal inhibitory concentration; LAMP: lysosomal associated membrane protein; LC3-II: phosphatidylethanolamine-conjugated form of MAP1LC3; LMP: lysosomal membrane permeabilization; MALDI: matrix assisted laser desorption ionization; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MKI67: marker of proliferation Ki-67; MTOR: mechanistic target of rapamycin kinase; MRI: magnetic resonance imaging; NH4Cl: ammonium chloride; NtBuHA: N-tert-butylhydroxylamine; PARP: poly(ADP-ribose) polymerase; PBS: phosphate-buffered saline; PPT1: palmitoyl-protein thioesterase 1; SD: standard deviation; SEM: standard error mean; vs, versus; Zn2+: zinc ion; Z-Phe: Z-Phe-Tyt(tBu)-diazomethylketone; Z-VAD-FMK: carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]- fluoromethylketone.
Insights
GNS561, a novel autophagy inhibitor, shows potent antitumor activity against liver cancer by inhibiting PPT1, leading to cell death. Its successful Phase 1b trial offers a promising new therapeutic strategy for hepatocellular carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Hepatocellular carcinoma (HCC) is the most common primary liver cancer.
- Existing autophagy inhibitors have not achieved clinical efficacy.
- GNS561 is a novel autophagy inhibitor with previously observed anticancer activity linked to lysosomal cell death.
Purpose of the Study:
- To evaluate the efficacy and mechanism of GNS561 in hepatocellular carcinoma.
- To investigate GNS561's liver tropism and antitumor activity.
- To explore GNS561's interaction with palmitoyl-protein thioesterase 1 (PPT1) and downstream effects.
Main Methods:
- In vitro testing against human cancer cell lines.
- In vivo studies using two hepatocellular carcinoma models.
- Analysis of lysosomal function, autophagic flux, and cell death pathways.
- Assessment of GNS561's enzyme target inhibition (PPT1).
Main Results:
- GNS561 demonstrated high liver tropism and potent antitumor effects in HCC models.
- GNS561 specifically inhibits PPT1, causing lysosomal zinc accumulation and impaired cathepsin activity.
- Inhibition of PPT1 by GNS561 blocked autophagic flux, induced lysosomal membrane permeabilization, and activated caspases, leading to cell death.
- A global Phase 1b clinical trial in liver cancers using GNS561 was successfully completed.
Conclusions:
- GNS561 is a promising drug candidate for liver cancer treatment.
- Its mechanism involves specific inhibition of PPT1, leading to lysosomal dysfunction and cancer cell death.
- GNS561 represents a hopeful therapeutic strategy, supported by successful clinical trial results.
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