ArticleProceedings of the National Academy of Sciences of the United States of America2025
The CYLD-PARP1 feedback loop regulates DNA damage repair and chemosensitivity in breast cancer cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Smyca-FOXM1 ribonucleoprotein complex promotes homologous recombination and tumor immune evasion to define a therapeutic target of triple-negative breast cancer.Journal of biomedical science · 2026Article
- DDX21 Promotes Breast Cancer Growth and Metastasis via Stimulating RNAPII Elongation During Hypoxia.MedComm · 2026Article
- Atox1 promotes CRC progression by protecting DNA damage through interacts with a novel copper-binding protein PARP1.Cell communication and signaling : CCS · 2026Article
- USP10 promotes cell proliferation and gemcitabine resistance in pancreatic cancer by the regulation of IGF2BP3-STEAP3.Oncogene · 2026Article
- NUSAP1 Recruits DAXX to Suppress HIF-Driven Triple-Negative Breast Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Poly(ADP-ribose) polymerase 1 (PARP1) plays a crucial role in DNA repair and genomic stability maintenance. However, the regulatory mechanisms governing PARP1 activity, particularly through deubiquitination, remain poorly elucidated. Using a deubiquitinase (DUB) library binding screen, we identified cylindromatosis (CYLD) as a bona fide DUB for PARP1 in breast cancer cells. Mechanistically, CYLD is recruited by PARP1 to DNA lesions upon genotoxic stress, where it cleaves K63-linked polyubiquitin chains on PARP1 at residues K748, K940, and K949, resulting in compromised PARP1 activation. In a reciprocal manner, PARP1 PARylates CYLD at sites E191, E231, E259, and E509, thereby enhancing its DUB activity. Consequently, depletion of CYLD leads to increased efficiency in base excision repair and confers breast cancer cells with resistance to alkylating agents. Conversely, overexpression of CYLD enhances sensitivity to PARP inhibitors (PARPi) even in homologous recombination-proficient breast cancer cells. These findings offer unique insights into the intricate interplay between CYLD and PARP1 in DNA repair, underscoring the pivotal role of targeting this regulatory axis for breast cancer chemotherapy.
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