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Genome-Wide Mapping of Histone Modifications and Transcription Factor Binding Sites in Neuroendocrine Small Cell Lung Cancer Cell Lines Using CUT&RUN
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Published on: April 3, 2026

Histone Methylation and Chromatin Remodeling in Non-Small Cell Lung Cancer: Mechanisms of Oncogenesis and Emerging

A Josephine Thrasher1, Omar Bushara1,2, Amy Gladstein2

  • 1Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA.

Biomedicines
|July 28, 2026
PubMed

Insights

Epigenetic modifiers play a key role in non-small cell lung cancer (NSCLC) development and treatment. Targeting these chromatin-modifying genes offers promising therapeutic strategies and potential biomarkers for NSCLC.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality, with poor survival rates for advanced stages despite current therapies.
  • Epigenetic modifiers, including chromatin-modifying genes, are increasingly recognized for their roles in NSCLC pathogenesis and therapeutic response.
  • Understanding these epigenetic alterations is crucial for developing novel treatment strategies.

Purpose of the Study:

  • To review key chromatin-modifying genes (writers, erasers, readers) implicated in non-small cell lung cancer (NSCLC).
  • To discuss the association of dysregulated epigenetic modifiers with NSCLC progression, metastasis, and treatment resistance.
  • To explore the potential of targeting epigenetic modifiers as therapeutic strategies and biomarkers for NSCLC.

Main Methods:

  • Literature review of chromatin-modifying genes (writers: KMT2A, SETD2, EZH2; erasers: KDM2, KDM5, KDM6 families; readers: SMARCA4, ARID1A) in NSCLC.
  • Analysis of the functional roles of these epigenetic modifiers in gene transcription, DNA accessibility, and tumor biology.
  • Survey of current clinical trials targeting epigenetic modifiers in NSCLC.

Main Results:

  • Dysregulation of writers, erasers, and readers is linked to NSCLC proliferation, metastasis, and resistance to therapies, including immunotherapy.
  • Emerging research highlights these genes as promising therapeutic targets and potential biomarkers for NSCLC.
  • Clinical trials are limited but show active development for SMARCA2 inhibitors in SMARCA4-mutated NSCLC and EZH2 inhibitors combined with PD-1 blockade.

Conclusions:

  • Epigenetic modifiers represent a critical area for NSCLC research, offering novel therapeutic avenues.
  • Targeting these genes may expand the treatment options for patients with advanced NSCLC.
  • Further investigation is warranted to fully elucidate their role and clinical utility in NSCLC management.
Keywords:
NSCLCepigenetic modifiersmethylation

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