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SMARCA4 regulates SMARCAD1 expression for toleration of replication stress in non-small cell lung cancer

Patinya Sawangsri1, Siripan Limsirichaikul1, Toshiyuki Takeuchi1

  • 1Department of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.

Fujita Medical Journal
|February 5, 2026
PubMed
Abstract

Insights

The SMARCA4-SMARCAD1 axis helps non-small cell lung cancer cells tolerate replication stress. SMARCA4 depletion increases SMARCAD1 expression, which is crucial for cell survival under stress.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • SMARCA4 mutations are common in non-small cell lung cancer (NSCLC).
  • SMARCA4 deficiency leads to replication stress and genomic instability.
  • SMARCAD1, a chromatin remodeler, is implicated in cancer development.

Purpose of the Study:

  • Investigate the SMARCA4-SMARCAD1 axis role in replication stress tolerance in NSCLC.
  • Determine the regulatory relationship between SMARCA4 and SMARCAD1 under replication stress.

Main Methods:

  • Utilized human NSCLC cell lines (Calu-6, NCI-H1975, Calu-1, NCI-H460).
  • Quantified SMARCA4 and SMARCAD1 expression via RT-PCR and immunoblotting.
  • Assessed SMARCAD1 localization at replication forks using immunofluorescence and transcriptional regulation via ChIP assays.

Main Results:

  • SMARCAD1 expression increased in SMARCA4-depleted cells under replication stress.
  • SMARCAD1 accumulated at stalled replication forks in SMARCA4-deficient cells.
  • SMARCA4 acts as a transcriptional suppressor of SMARCAD1, binding its regulatory region.

Conclusions:

  • The SMARCA4-SMARCAD1 axis is a novel mechanism for replication stress tolerance.
  • Both SMARCA4 and SMARCAD1 are essential for NSCLC cell survival under replication stress.
Keywords:
NSCLCReplication stressSMARCA4SMARCAD1

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