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Master Transcription Factor Reprogramming Unleashes Selective Translation Promoting Castration Resistance and Immune

Sandra Santasusagna1,2, Shijia Zhu3,4, Vijayakumar Jawalagatti1,2

  • 1Department of Urology, Mayo Comprehensive Cancer Center, Rochester, Minnesota.

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Summary

In lethal prostate cancer, reduced microphthalmia transcription factor (MITF) allows eIF3B to reprogram translation, driving resistance to androgen deprivation therapy (ADT) and immune evasion. Targeting this pathway sensitizes tumors to ADT and immunotherapy.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Tumor cells rewire signaling pathways to survive therapy.
  • Lethal prostate cancer exhibits resistance to androgen deprivation therapy (ADT) and immune evasion.

Purpose of the Study:

  • To investigate the role of microphthalmia transcription factor (MITF) in prostate cancer therapy resistance.
  • To elucidate the mechanism of eIF3B-mediated translation reprogramming in conferring resistance and immune evasion.

Main Methods:

  • Direct promoter binding assays to study MITF-eIF3B interaction.
  • Genome-wide eIF3B enhanced cross-linking immunoprecipitation sequencing (eCLIP-seq) to identify binding sites.
  • Preclinical models to test pharmacologic targeting of eIF3B-dependent translation.

Main Results:

  • Downregulation of MITF unleashes eIF3B-dependent translation of key mRNAs.
  • eIF3B binds to a UC-rich motif in 5' untranslated regions, regulating translation of androgen receptor and MHC-I.
  • Pharmacologic targeting of eIF3B sensitizes prostate cancer to ADT and anti-PD-1 therapy.

Conclusions:

  • MITF-eIF3B axis represents a critical link between transcriptional and translational control in therapy-refractory prostate cancer.
  • Targeting eIF3B-dependent translation offers a druggable strategy to overcome ADT resistance and enhance immunotherapy efficacy.