Evidence map›Paper›PMID 41641123›Full record

ArticleFujita medical journal2026

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

Patinya Sawangsri, Siripan Limsirichaikul, Toshiyuki Takeuchi, Yasuyoshi Mizutani, Dat Quoc Tran, Taisuke Kajino, Motoshi Suzuki, Atsuko Niimi

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In one paragraph

Article in Fujita medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Patinya SawangsriDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Siripan LimsirichaikulDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Toshiyuki TakeuchiDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Yasuyoshi MizutaniDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Dat Quoc TranDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Taisuke KajinoDivision of Molecular Diagnostics, Aichi Cancer Center Research Institute, Nagoya, Aichi, Japan.
Motoshi SuzukiDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Atsuko NiimiDepartment of Molecular Oncology, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: SMARCA4, a core component of the SWI/SNF chromatin remodeling complex, is frequently mutated in non-small cell lung cancer (NSCLC). SMARCA4-deficient cancer cells are associated with increased replication stress, one of the major causes of genomic instability, which may lead to cancer. SMARCAD1, a chromatin remodeler, is known as replication fork progressor, and SMARCAD1 dysregulation is also closely related to cancer development. This study aimed to investigate the role of the SMARCA4-SMARCAD1 axis in the toleration of replication stress in NSCLC, focusing on the regulatory relationship between SMARCA4 and SMARCAD1 during replication stress conditions. Methods: Human NSCLC cell lines (Calu-6, NCI-H1975, Calu-1, and NCI-H460) were used for experiments. SMARCA4 and SMARCAD1 expression levels were analyzed by quantitative RT-PCR and immunoblotting. Transcriptional regulation of SMARCAD1 was analyzed by chromatin immunoprecipitation assay. Immunofluorescent analysis was performed to assess SMARCAD1 accumulation at stalled replication forks. Clonogenic assays were conducted to evaluate the roles of SMARCA4 and SMARCAD1 in cell survival. Results: SMARCAD1 was highly expressed in SMARCA4-depleted cells under replication stress. Immunofluorescent analysis revealed significant accumulation of SMARCAD1 at stalled replication forks in SMARCA4-depleted cells. Chromatin immunoprecipitation assays demonstrated that SMARCA4 bound to the transcriptional regulatory region of Conclusions: The SMARCA4-SMARCAD1 axis is a novel mechanism that provides tolerance for replication stress.

Indexed as

NSCLCReplication stressSMARCA4SMARCAD1

Identifiers

PMID41641123
PMCPMC12865287

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.