ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancer Article Swipe
Sara Lago
,
Vittoria Poli
,
Lisa Fol
,
Mattia Botteon
,
Federica Busi
,
Alice Turdo
,
Miriam Gaggianesi
,
Yari Ciani
,
Giuseppe D’Amato
,
Luca Fagnocchi
,
Alessandra Fasciani
,
Francesca Demichelis
,
Matilde Todaro
,
Alessio Zippo
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41467-025-59804-0
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41467-025-59804-0
Oncogene-induced replicative stress (RS) drives tumor progression by disrupting genome stability, primarily through transcription-replication conflicts (TRCs), which promote R-loop accumulation and trigger the DNA damage response (DDR). In this study, we investigate the role of chromatin regulators in exacerbating TRCs and R-loop accumulation in cancer. We find that in breast cancer patients, the simultaneous upregulation of MYC and the H2A.Z-specific chaperone ANP32E correlates with increased genomic instability. Genome-wide analyses reveal that ANP32E-driven H2A.Z turnover alters RNA polymerase II processivity, leading to the accumulation of long R-loops at TRC sites. Furthermore, we show that ANP32E overexpression enhances TRC formation and activates an ATR-dependent DDR, predisposing cancer cells to R-loop-mediated genomic fragility. By exploiting the vulnerability of ANP32E-expressing cancer cells to ATR inhibitors, we find that tumors relied on this DDR pathway, whose inhibition halts their pro-metastatic capacity. These findings identify ANP32E as a key driver of TRC-induced genomic instability, indicating ATR inhibition as a potential therapeutic strategy for ANP32E-overexpressing tumors.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1038/s41467-025-59804-0
- https://www.nature.com/articles/s41467-025-59804-0.pdf
- OA Status
- gold
- Cited By
- 1
- References
- 102
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4410457060
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Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4410457060Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1038/s41467-025-59804-0Digital Object Identifier
- Title
-
ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancerWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-05-17Full publication date if available
- Authors
-
Sara Lago, Vittoria Poli, Lisa Fol, Mattia Botteon, Federica Busi, Alice Turdo, Miriam Gaggianesi, Yari Ciani, Giuseppe D’Amato, Luca Fagnocchi, Alessandra Fasciani, Francesca Demichelis, Matilde Todaro, Alessio ZippoList of authors in order
- Landing page
-
https://doi.org/10.1038/s41467-025-59804-0Publisher landing page
- PDF URL
-
https://www.nature.com/articles/s41467-025-59804-0.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://www.nature.com/articles/s41467-025-59804-0.pdfDirect OA link when available
- Concepts
-
Triple-negative breast cancer, Replication (statistics), Breast cancer, Transcription (linguistics), Vulnerability (computing), Biology, Transcription factor, Cancer research, Cell biology, Computational biology, Genetics, Cancer, Gene, Computer science, Virology, Computer security, Linguistics, PhilosophyTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
1Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 1Per-year citation counts (last 5 years)
- References (count)
-
102Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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