ArticleCancer research2021
Combinatorial CRISPR/Cas9 Screening Reveals Epistatic Networks of Interacting Tumor Suppressor Genes and Therapeutic Targets in Human Breast Cancer.
Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Network-based analysis reveals potential microRNA regulation of oncogenic pathways in SOX10-depleted uveal melanoma.Cellular and molecular life sciences : CMLS · 2026Article
- CRISPR/Cas9 Genome Editing in Oncology: Mechanisms, Therapeutic Platforms and Translational Challenges.Molecular biotechnology · 2026Review
- Insights from pooled CRISPRi single-cell screens in K562 cells reveal gene functions, regulatory networks, and highlight opportunities and limitations.BMC genomics · 2026Article
- Large-scale mapping of environmental-genetic interactions illustrates the dynamic nature of cell-cycle and DNA repair regulation.Molecular cell · 2026Article
- Using Biological Networks to Guide Biomedical Prediction.Methods in molecular biology (Clifton, N.J.) · 2026Article
- CRISPR screening approaches in breast cancer research.Cancer metastasis reviews · 2025Review
- Genetic advancements in breast cancer treatment: a review.Discover oncology · 2025Review
- Combinatorial In Vivo Genome Editing Identifies Widespread Epistasis and an Accessible Fitness Landscape During Lung Tumorigenesis.Molecular biology and evolution · 2025Article
- CRISPR/Cas9 technology in tumor research and drug development application progress and future prospects.Frontiers in pharmacology · 2025Review
- Considerations in the search for epistasis.Genome biology · 2024Review
- CRISPR-Cas and CRISPR-based screening system for precise gene editing and targeted cancer therapy.Journal of translational medicine · 2024Review
- SRPK1 Promotes Glioma Proliferation, Migration, and Invasion through Activation of Wnt/β-Catenin and JAK-2/STAT-3 Signaling Pathways.Biomedicines · 2024Article
- Synthetic viability induces resistance to immune checkpoint inhibitors in cancer cells.British journal of cancer · 2023Article
- Applications of CRISPR Technology to Breast Cancer and Triple Negative Breast Cancer Research.Cancers · 2023Review
- Massively Parallel CRISPR-Based Genetic Perturbation Screening at Single-Cell Resolution.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- A CRISPR Path to Finding Vulnerabilities and Solving Drug Resistance: Targeting the Diverse Cancer Landscape and Its Ecosystem.Advanced genetics (Hoboken, N.J.) · 2022Review
- Identifying driver modules based on multi-omics biological networks in prostate cancer.IET systems biology · 2022Article
- Strategies to overcome the main challenges of the use of CRISPR/Cas9 as a replacement for cancer therapy.Molecular cancer · 2022Review
- LINA: A Linearizing Neural Network Architecture for Accurate First-Order and Second-Order Interpretations.IEEE access : practical innovations, open solutions · 2022Article
- It's Getting Complicated-A Fresh Look at p53-MDM2-ARF Triangle in Tumorigenesis and Cancer Therapy.Frontiers in cell and developmental biology · 2022Review
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4 authors at 2 institutions in 1 country.
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Abstract
The majority of cancers are driven by multiple genetic alterations, but how these changes collaborate during tumorigenesis remains largely unknown. To gain mechanistic insights into tumor-promoting genetic interactions among tumor suppressor genes (TSG), we conducted combinatorial CRISPR screening coupled with single-cell transcriptomic profiling in human mammary epithelial cells. As expected, different driver gene alterations in mammary epithelial cells influenced the repertoire of tumor suppressor alterations capable of inducing tumor formation. More surprisingly, TSG interaction networks were comprised of numerous cliques-sets of three or four genes such that each TSG within the clique showed oncogenic cooperation with all other genes in the clique. Genetic interaction profiling indicated that the predominant cooperating TSGs shared overlapping functions rather than distinct or complementary functions. Single-cell transcriptomic profiling of CRISPR double knockouts revealed that cooperating TSGs that synergized in promoting tumorigenesis and growth factor independence showed transcriptional epistasis, whereas noncooperating TSGs did not. These epistatic transcriptional changes, both buffering and synergistic, affected expression of oncogenic mediators and therapeutic targets, including CDK4, SRPK1, and DNMT1. Importantly, the epistatic expression alterations caused by dual inactivation of TSGs in this system, such as
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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.