ArticleCell cycle (Georgetown, Tex.)2016
MYC interaction with the tumor suppressive SWI/SNF complex member INI1 regulates transcription and cellular transformation.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Canonical BAF chromatin remodeling complex specifies stem cell fate via cell-type-specific co-factor recruitment.Nature communications · 2026Article
- The LFR-SWI/SNF complex: A chromatin wrench safeguarding cellular quiescence in theProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular and therapeutic landscape of non-clear cell renal carcinoma.Nature reviews. Urology · 2025Review
- Reoviruses hijack the SMARCB1-MYC transcriptional regulation complex to activate autophagy for persistent viral infection in leafhopper vector.PLoS pathogens · 2025Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- SMARCB1 Gene Therapy Using a Novel Tumor-Targeted Nanomedicine Enhances Anti-Cancer Efficacy in a Mouse Model of Atypical Teratoid Rhabdoid Tumors.International journal of nanomedicine · 2024Article
- Advances in the role of SWI/SNF complexes in tumours.Journal of cellular and molecular medicine · 2023Review
- Article
- Polyploidy and Myc Proto-Oncogenes Promote Stress Adaptation via Epigenetic Plasticity and Gene Regulatory Network Rewiring.International journal of molecular sciences · 2022Review
- Review
- Review
- Article
- The SWI/SNF ATPase BRG1 facilitates multiple pro-tumorigenic gene expression programs in SMARCB1-deficient cancer cells.Oncogenesis · 2022Article
- Emerging Themes in Mechanisms of Tumorigenesis by SWI/SNF Subunit Mutation.Epigenetics insights · 2022Review
- Article
- MYC protein interactors in gene transcription and cancer.Nature reviews. Cancer · 2021Review
- Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler.Oncogene · 2021Article
- Emerging role of SWI/SNF complex deficiency as a target of immune checkpoint blockade in human cancers.Oncogenesis · 2021Review
- The core SWI/SNF catalytic subunit Brg1 regulates nephron progenitor cell proliferation and differentiation.Developmental biology · 2020Article
- Comprehensive Molecular Characterization Identifies Distinct Genomic and Immune Hallmarks of Renal Medullary Carcinoma.Cancer cell · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
MYC is a key driver of cellular transformation and is deregulated in most human cancers. Studies of MYC and its interactors have provided mechanistic insight into its role as a regulator of gene transcription. MYC has been previously linked to chromatin regulation through its interaction with INI1 (SMARCB1/hSNF5/BAF47), a core member of the SWI/SNF chromatin remodeling complex. INI1 is a potent tumor suppressor that is inactivated in several types of cancers, most prominently as the hallmark alteration in pediatric malignant rhabdoid tumors. However, the molecular and functional interaction of MYC and INI1 remains unclear. Here, we characterize the MYC-INI1 interaction in mammalian cells, mapping their minimal binding domains to functionally significant regions of MYC (leucine zipper) and INI1 (repeat motifs), and demonstrating that the interaction does not interfere with MYC-MAX interaction. Protein-protein interaction network analysis expands the MYC-INI1 interaction to the SWI/SNF complex and a larger network of chromatin regulatory complexes. Genome-wide analysis reveals that the DNA-binding regions and target genes of INI1 significantly overlap with those of MYC. In an INI1-deficient rhabdoid tumor system, we observe that with re-expression of INI1, MYC and INI1 bind to common target genes and have opposing effects on gene expression. Functionally, INI1 re-expression suppresses cell proliferation and MYC-potentiated transformation. Our findings thus establish the antagonistic roles of the INI1 and MYC transcriptional regulators in mediating cellular and oncogenic functions.
Indexed as
Identifiers
What OpenQuestion holds
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.