ArticleMolecular oncology2023
CRISPR/Cas9 screen for genome-wide interrogation of essential MYC-bound E-boxes in cancer cells.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- The Growth Supporting Role of ZDHHC11 Is Linked to the MEF2B-BCL6 Regulatory Circuit in Burkitt Lymphoma.International journal of cancer · 2026Article
- CRISPR/Cas9 in Cancer Therapy: Precision Genome Editing Approaches Targeting Hematological Malignancies and Solid Tumors Through Cellular, Biochemical, and Molecular Mechanisms.Cell biochemistry and biophysics · 2026Review
- CRISPR-Cas9 screen reveals that inhibition of enhancer of zeste homolog 2 sensitizes malignant T cells to dimethyl-fumarate-induced cell death.The FEBS journal · 2026Article
- Comparative Analysis of Methods for Assessing On-Target Gene Editing Efficiencies.Methods and protocols · 2025Article
- AZIN1 level is increased in medulloblastoma and correlates with c-Myc activity and tumor phenotype.Journal of experimental & clinical cancer research : CR · 2025Article
- Genetic advancements in breast cancer treatment: a review.Discover oncology · 2025Review
- Inhibition of the glutamate-cysteine ligase catalytic subunit with buthionine sulfoximine enhances the cytotoxic effect of doxorubicin and cyclophosphamide in Burkitt lymphoma cells.Journal of applied genetics · 2024Article
- Mitochondrial fatty acid synthesis is an emergent central regulator of mammalian oxidative metabolism.Cell metabolism · 2024Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcription factor MYC is a proto-oncogene with a well-documented essential role in the pathogenesis and maintenance of several types of cancer. MYC binds to specific E-box sequences in the genome to regulate gene expression in a cell-type- and developmental-stage-specific manner. To date, a combined analysis of essential MYC-bound E-boxes and their downstream target genes important for growth of different types of cancer is missing. In this study, we designed a CRISPR/Cas9 library to destroy E-box sequences in a genome-wide fashion. In parallel, we used the Brunello library to knock out protein-coding genes. We performed high-throughput screens with these libraries in four MYC-dependent cancer cell lines-K562, ST486, HepG2, and MCF7-which revealed several essential E-boxes and genes. Among them, we pinpointed crucial common and cell-type-specific MYC-regulated genes involved in pathways associated with cancer development. Extensive validation of our approach confirmed that E-box disruption affects MYC binding, target-gene expression, and cell proliferation in vitro as well as tumor growth in vivo. Our unique, well-validated tool opens new possibilities to gain novel insights into MYC-dependent vulnerabilities in cancer cells.
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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.