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Context‑dependent targeting of thioredoxin reductase 1 in cancer: a mechanistic review

Beáta Biri-Kovács1, Katalin Úri1, Attila Andor1

  • 1Department of Selenoprotein Research and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary. elias.arner@oncol.hu.

Magyar Onkologia
|May 31, 2026
PubMed

Insights

Targeting thioredoxin reductase 1 (TrxR1) shows promise for cancer treatment but has context-dependent outcomes. This study links TrxR1

Area of Science:

  • Oncology
  • Redox Biology
  • Cancer Therapeutics

Background:

  • Thioredoxin reductase 1 (TrxR1) is a key cytosolic selenoprotein.
  • Targeting TrxR1 exploits cancer-specific redox vulnerabilities.
  • TrxR1 inhibition exhibits context-dependent outcomes in cancer treatment.

Purpose of the Study:

  • To synthesize a mechanistic framework for TrxR1 inhibition in cancer.
  • To link cytosolic redox buffering, proteostasis, RTK signaling, and immune surveillance to treatment responses.
  • To explore combination strategies involving TrxR1 modulators.

Main Methods:

  • Mechanistic synthesis of preclinical and clinical data.
  • Analysis of TrxR1-substrate interactions, including TXNL1.
  • Investigation of intracellular transcriptional crosstalk.
  • Evaluation of combination strategies with RTK modulators.

Main Results:

  • A framework linking TrxR1 activity to cancer treatment response is established.
  • The dual roles of TrxR1-substrate TXNL1 (TRP32) are highlighted.
  • Intracellular transcriptional crosstalk significantly influences treatment sensitivity.
  • Potential synergistic effects with RTK modulators are outlined.

Conclusions:

  • TrxR1 inhibition is a complex cancer therapy strategy.
  • Understanding the interplay between redox, proteostasis, signaling, and immunity is crucial.
  • Combination therapies targeting TrxR1 and RTKs may improve treatment efficacy.

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