ArticleNature communications2019
A requirement for STAG2 in replication fork progression creates a targetable synthetic lethality in cohesin-mutant cancers.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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.
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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
80 citing papers in PubMed, 109 citations in OpenAlex.
- Folding a broken genome: the versatile roles of cohesin in genome maintenance.Nature reviews. Genetics · 2026Review
- Three-dimensional chromatin architecture is rapidly restored after DNA replication.Nature communications · 2026Article
- Contribution of cohesins STAG1 and STAG2 to preimplantation development in mice.Communications biology · 2026Article
- DNA replication stress and translational repression converge to drive CDK1- and caspase-dependent apoptosis in Ewing sarcoma.Oncogene · 2026Article
- Outcomes of patients with or without DNA repair pathway alterations: the MD Anderson IMPACT2 study.NPJ precision oncology · 2026Article
- Novel variants inExperimental and therapeutic medicine · 2026Article
- Epigenetic Regulation of Higher-Order Chromatin Structure (HOCS) and Its Implication in Human Diseases.Cancers · 2026Review
- Cohesin mutations and chromatin changes in cancer.International journal of cancer · 2026Review
- Assessing SMC Complex Function in Replication Fork Progression with DNA Fiber Assays.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Tumor-suppressive activities of SA1/STAG2 and effects of PARP impairment during brain development.Disease models & mechanisms · 2026Article
- S-phase PARylation of microprotein RSMC enhances the function of Sororin in sister chromatid cohesion.The EMBO journal · 2026Article
- The Puzzle of Genetic Stability and Chromosomal Copy Number Alterations for the Therapy of Ewing Sarcoma.Cancers · 2025Review
- Robust CENP-A incorporation in human cells is independent of transcription and cohesin components.Molecular biology of the cell · 2025Article
- Mitigating Cell Cycle Effects in Multi-Omics Data: Solutions and Analytical Frameworks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Histone Deacetylase Inhibitors Target DNA Replication Regulators and Replication Stress in Ewing Sarcoma Cells.Cancer research communications · 2025Article
- Co-essentiality analysis identifies PRR12 as a cohesin interacting protein and contributor to genomic integrity.Developmental cell · 2025Article
- HDAC2-Mediated METTL3 Delactylation Promotes DNA Damage Repair and Chemotherapy Resistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- STAG2 expression imparts distinct therapeutic vulnerabilities in muscle-invasive bladder cancer cells.Oncogenesis · 2025Article
- Emerging roles of cohesin-STAG2 in cancer.Oncogene · 2025Review
- A STAG2-PAXIP1/PAGR1 axis suppresses lung tumorigenesis.The Journal of experimental medicine · 2025Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cohesin is a multiprotein ring that is responsible for cohesion of sister chromatids and formation of DNA loops to regulate gene expression. Genomic analyses have identified that the cohesin subunit STAG2 is frequently inactivated by mutations in cancer. However, the reason STAG2 mutations are selected during tumorigenesis and strategies for therapeutically targeting mutant cancer cells are largely unknown. Here we show that STAG2 is essential for DNA replication fork progression, whereby STAG2 inactivation in non-transformed cells leads to replication fork stalling and collapse with disruption of interaction between the cohesin ring and the replication machinery as well as failure to establish SMC3 acetylation. As a consequence, STAG2 mutation confers synthetic lethality with DNA double-strand break repair genes and increased sensitivity to select cytotoxic chemotherapeutic agents and PARP or ATR inhibitors. These studies identify a critical role for STAG2 in replication fork procession and elucidate a potential therapeutic strategy for cohesin-mutant cancers.
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Registered trials
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.