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April 5, 2026Cancer Research

Cysteine Accumulation Drives Resistance To Bortezomib In Cancer Treatment

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Authors

JBJennifer A. BrainSCS. S. ChangMKMaximilian Kobiesa

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Overview

High cysteine levels enhance resistance to bortezomib in cancer cells, suggesting therapeutic implications.

Key Points

  • This research aims to explore how cysteine levels affect resistance to bortezomib and related proteasome inhibitors.
  • Conducted a high throughput screen of chemotherapeutics under varying cysteine conditions.
  • Measured resistance to bortezomib and related inhibitors in cancer cell lines.
  • Used LC-MS to confirm covalent conjugation between cysteine and drugs.
  • Altered cysteine levels using agents like NAC and erastin to test sensitivity changes.
  • Cells showed greater resistance to bortezomib and ixazomib under high cysteine conditions.
  • Cysteine was found to form a covalent conjugate with bortezomib, reducing drug toxicity.
  • Resistance to carfilzomib was unaffected by cysteine levels, indicating a unique interaction with boronic acid inhibitors.
  • Decreasing intracellular cysteine levels increased sensitivity to bortezomib and ixazomib.
  • High cysteine levels impaired proteasome function in cells treated with boronic acid inhibitors.

Cite This Study

Brain et al. (2026) studied this question.

synapsesocial.com/papers/69d1fe68a79560c99a0a4ae4https://doi.org/10.1158/1538-7445.am2026-1788
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Abstract 379: Cysteine-driven drug inactivation undermines covalent drug efficacy and drives resistance.2026
  2. 2Abstract LB349: Cysteine restriction enhances antitumor immunity in colorectal cancer2024
  3. 3Abstract 436: Extracellular glutathione catabolism as an alternative cyst(e)ine source in cancer2024 · 1 citations
  4. 4Abstract 1272: Targeting autophagy sensitizes cancer cells to proteasome inhibitors.2026
  5. 5Abstract LB293: Cystine restriction enhances CD8+ CAR-T potency by promoting OXPHOS via GCN2-eIF2α-SLC1A5 axis2026