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Mechanisms of GZ17-6.02 resistance

Laurence Booth1, Cameron West2, Daniel Von Hoff3

  • 1Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, Virginia.

Anti-Cancer Drugs
|March 11, 2022
PubMed
Abstract

Insights

The drug GZ17-6.02 shows promise for colon cancer treatment, enhancing anti-PD1 antibody efficacy. Resistance mechanisms involving ERBB signaling were identified, and histone deacetylase (HDAC) inhibitors reversed this resistance.

Area of Science:

  • Oncology
  • Cancer Biology
  • Pharmacology

Background:

  • GZ17-6.02 is an investigational drug in phase I clinical trials for solid tumors.
  • Colorectal cancer (CRC) remains a significant health concern, necessitating novel therapeutic strategies.
  • Understanding drug resistance mechanisms is crucial for optimizing cancer treatment efficacy.

Purpose of the Study:

  • To evaluate the impact of prolonged GZ17-6.02 exposure on colorectal tumors.
  • To determine if GZ17-6.02 enhances the efficacy of anti-PD1 antibody therapy.
  • To elucidate the mechanisms of acquired resistance to GZ17-6.02 in tumor cells.

Main Methods:

  • In vivo animal studies utilizing colorectal tumor models.
  • Cellular assays including immunoblotting, transfection, and trypan blue death assays.
  • Analysis of signaling pathway activation and protein expression in resistant tumor cells.

Main Results:

  • GZ17-6.02 prolonged survival by enhancing 5-fluorouracil and anti-PD1 antibody efficacy.
  • Acquired resistance involved upregulation of ERBB2/ERBB3 and altered phosphorylation of key signaling proteins.
  • Histone deacetylase (HDAC) inhibition reversed GZ17-6.02 resistance by restoring CD95 and FAS-L levels.

Conclusions:

  • GZ17-6.02 demonstrates therapeutic potential for colon cancer.
  • Acquired resistance to GZ17-6.02 can be overcome with combination therapy involving HDAC inhibitors.
  • Further development of GZ17-6.02, potentially with HDAC inhibitors, is warranted for colon cancer treatment.

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