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Related Concept Videos

Cells of the Adaptive Immune Response01:23

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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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Preparation of Aplysia Sensory-motor Neuronal Cell Cultures
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AP-1 mediates cellular adaptation and memory formation.

Jingxin Li1, Pavithran T Ravindran2, Aoife O'Farrell3

  • 1Genetics and Epigenetics, Cell and Molecular Biology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Nature Communications
|March 21, 2026
PubMed
Summary
This summary is machine-generated.

Cancer cells develop drug resistance by forming cellular memories, a process linked to the transcription factor AP-1. This cellular learning enables adaptation to therapy, highlighting a new aspect of gene regulation in treatment resistance.

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Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • Cellular responses are traditionally viewed as genetically programmed.
  • The mechanisms underlying therapy resistance in cancer are not fully understood.

Purpose of the Study:

  • To investigate the role of cellular memory in cancer drug resistance.
  • To identify the molecular factors involved in establishing and maintaining therapy-induced cellular memory.

Main Methods:

  • Utilized a two-color AP-1 reporter system in cancer cells.
  • Analyzed gene expression patterns following low-dose therapy exposure.
  • Assessed chromatin accessibility changes.
  • Investigated the role of the transcription factor AP-1.

Main Results:

  • Cancer cells form and maintain drug resistance through cellular memories.
  • This cellular learning is dependent on the transcription factor AP-1.
  • Therapy application encodes transient gene expression into stable cellular memory.
  • Memories are encoded in cis, demonstrating activating cis-epigenetics.
  • Chromatin accessibility persists along with cellular memory.

Conclusions:

  • Cellular memory formation is a critical mechanism in the development of cancer therapy resistance.
  • AP-1 mediated gene regulation plays a key role in establishing these memories.
  • Findings reveal a novel layer of gene regulation involving epigenetic memory in cancer adaptation.