Evidence map›Paper›PMID 42524029›Full record

ArticleFrontiers in oncology2026

Transcriptomic differences in chromatin and cell cycle regulation in A549 cells after irradiation with carbon ions and X-rays.

Hasan Nisar, Özdemirhan Serçin, Christine E Hellweg

Abstract read
In one paragraph

Article in Frontiers in oncology, 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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Hasan NisarDepartment of Radiation Biology, Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany.
Özdemirhan SerçinDepartment of Radiation Biology, Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany.
Christine E HellwegDepartment of Radiation Biology, Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: High-linear energy transfer (LET) radiation such as carbon ions exhibits greater biological effectiveness than conventional low-LET X-rays, but the transcriptional mechanisms underlying this advantage remain incompletely understood. We hypothesized that high-LET radiation induces a qualitatively different transcriptional response rather than simply amplifying low-LET signaling. Methods: A549 non-small cell lung cancer cells were exposed to equal physical doses (8 Gy) of X-rays or carbon ions (LET 73 keV/µm), and transcriptomic profiling was performed 4 h post-irradiation. Differential expression analysis was integrated with Hallmark pathway enrichment using gene set enrichment analysis (GSEA), over-representation analysis (ORA), and leading-edge gene interrogation to identify shared and LET-dependent gene expression regulation. Results: Both radiation modalities activated a conserved DNA damage response characterized by p53 signaling and apoptosis-related genes. In contrast, carbon ions selectively suppressed mitotic regulators including CENPE, KIF2C, PLK1, and BUB1, consistent with transcriptional disruption of the replication-segregation machinery. High-LET irradiation additionally enriched inflammatory and stress-associated pathways, including tumor necrosis factor (TNF), Nuclear Factor κB (NF-κB) and extracellular matrix and adhesion-related signatures annotated within the Hallmark epithelial-mesenchymal transition (EMT) gene set. Carbon ions also downregulated multiple core and linker histone genes, revealing a chromatin regulatory reprogramming signature although this may reflect modulation of mRNA stability linked to replication stress and cell-cycle progression. KRAS-associated gene networks were enriched under high-LET conditions, reflecting convergence of stress-responsive signaling. Discussion: At equal physical doses, high-LET carbon ion irradiation is associated with a transcriptional program distinct from that of low-LET X-rays, characterized by downregulation of mitotic and chromatin regulatory programs and selective engagement of stress-associated signaling networks. These findings provide mechanistic insight into LET-dependent radiobiology and suggest transcriptional pathway remodeling may contribute to the enhanced biological effectiveness of carbon ions.

Indexed as

A549 lung cancercell cycle regulationchromatin regulatory reprogrammingDNA damage responsegene set enrichment analysis (GSEA)high-LET radiationRNA sequencing

Identifiers

PMID42524029
PMCPMC13408517

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