Targeting ADAR1 with a small molecule for the treatment of prostate cancer

Nat Cancer. 2025 Mar;6(3):474-492. doi: 10.1038/s43018-025-00907-4. Epub 2025 Feb 10.

Abstract

Despite the initial response to androgen signaling therapy, most cases of prostate cancer (PCa) eventually relapse and remain incurable. The specific function of ADAR1 that governs PCa progression and specific inhibitors of ADAR are underexplored. In this study, we demonstrate that highly expressed ADAR1 is a crucial oncogenic target in PCa and develop an effective small-molecule ADAR1 inhibitor, ZYS-1, with marked antitumor efficacy and a favorable safety profile. Either genetic or pharmacological inhibition of ADAR1 dramatically suppressed PCa growth and metastasis and potentiated the antitumor immune response. Moreover, ZYS-1 can enhance the antitumor effect of immunotherapy. We also reveal that ADAR1 represses the translation of MTDH in an editing-dependent manner, which drives cell proliferation and invasion in PCa. Collectively, our findings suggest that ADAR1 is a druggable target in PCa and highlight the widespread applicability of ADAR1 inhibitors for a broad spectrum of malignancies.

MeSH terms

  • Adenosine Deaminase* / genetics
  • Adenosine Deaminase* / metabolism
  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Cell Line, Tumor
  • Cell Proliferation* / drug effects
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Immunotherapy / methods
  • Male
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mice
  • Prostatic Neoplasms* / drug therapy
  • Prostatic Neoplasms* / genetics
  • Prostatic Neoplasms* / metabolism
  • Prostatic Neoplasms* / pathology
  • RNA-Binding Proteins* / metabolism
  • Xenograft Model Antitumor Assays

Substances

  • Adenosine Deaminase
  • RNA-Binding Proteins
  • ADAR protein, human
  • Membrane Proteins
  • MTDH protein, human
  • Antineoplastic Agents