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Cancer pathogenesis and phase targeting through condensate fragility.

Menghua Wang1, Takudzwa Chiwoneso2, Zimeng Luo2

  • 1State Key Laboratory of Natural Medicines, Department of Natural Medicinal Chemistry, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 639 Longmian Avenue, Nanjing 211198, China; Department of Chemistry, The University of British Columbia, Vancouver, BC V6T 1Z1, Canada.

Trends in Pharmacological Sciences
|March 7, 2026
PubMed
Summary
This summary is machine-generated.

Nuclear liquid-liquid phase separation (LLPS) organizes cell functions. Aberrant LLPS in cancer creates fragile condensates, offering a new therapeutic target by exploiting their instability.

Keywords:
condensate fragilitygenomic instabilitynuclear liquid–liquid phase separationphase targetingtranscriptional dysregulation

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Area of Science:

  • Molecular Biology
  • Biophysics
  • Cancer Research

Background:

  • Nuclear liquid-liquid phase separation (LLPS) organizes transcription and DNA repair into dynamic condensates, crucial for genome integrity.
  • Dysregulated LLPS is a key driver of oncogenesis, but its role in promoting both transcriptional addiction and genomic instability is not fully understood.

Purpose of the Study:

  • To review the role of aberrant nuclear LLPS in cancer pathogenesis and therapy resistance.
  • To propose phase targeting through condensate fragility as a precision oncology strategy.

Main Methods:

  • Review of recent biophysical and molecular advances in LLPS.
  • Analysis of how cancer-associated mutations affect condensate properties.
  • Integration of oncogenic mechanisms with biophysical vulnerabilities.

Main Results:

  • Cancer-associated mutations rewire LLPS to form hyperstable yet fragile condensates.
  • Aberrant nuclear LLPS contributes to both transcriptional addiction and genomic instability in cancer.

Conclusions:

  • Targeting the fragility of aberrant nuclear condensates presents a novel precision oncology strategy.
  • This approach integrates oncogenic mechanisms with actionable biophysical vulnerabilities for cancer therapy.