ArticleThe Journal of clinical investigation2016
CCAT1 is an enhancer-templated RNA that predicts BET sensitivity in colorectal cancer.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
139 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.
- Prognostic value of long non-coding RNA CCAT1 expression in patients with cancer: A meta-analysis.PloS one · 2017Pooled it
- Subtype-specific enhancer RNAs define transcriptional regulators and prognosis in breast cancers.Molecular oncology · 2026Article
- BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition.Cellular & molecular biology letters · 2026Article
- BET inhibition disrupts the FOXM1-MYC axis to induce BRCAness and enhance PARP inhibitor response.NPJ precision oncology · 2026Article
- Deciphering the regulatory landscape of enhancer RNAs in health and disease.Signal transduction and targeted therapy · 2026Review
- HDAC7-Induced Epigenetic Repression Modulates ATF3 Functional Plasticity in Colorectal Cancer Pathogenesis.International journal of biological sciences · 2026Article
- Article
- BRD2 Upregulation as a Pan-Cancer Adaptive Resistance Mechanism to BET Inhibition.bioRxiv : the preprint server for biology · 2025Article
- The histone modifier KAT2A presents a selective target in a subset of well-differentiated microsatellite-stable colorectal cancers.Cell death and differentiation · 2025Article
- Enhancer RNAs profiling in colorectal cancer liver metastases reveals novel molecular subtypes with prognostic and therapeutic relevance.Discover oncology · 2025Article
- Enhancer RNA Transcriptome-Wide Association Study Reveals a Distinctive Class of Pan-Cancer Susceptibility eRNAs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Epigenetic marvels: exploring the landscape of colorectal cancer treatment through cutting-edge epigenetic-based drug strategies.Clinical epigenetics · 2025Review
- Inhibition of BRD4 attenuated IFNγ-induced apoptosis in colorectal cancer organoids.BMC cancer · 2025Article
- Application Strategies of Super-Enhancer RNA in Cardiovascular Diseases.Biomedicines · 2025Review
- Bromodomain-containing 4 as a therapeutic target in inflammatory bowel diseases and colorectal cancer.Frontiers in pharmacology · 2025Review
- eRNA-IDO: A One-stop Platform for Identification, Interactome Discovery, and Functional Annotation of Enhancer RNAs.Genomics, proteomics & bioinformatics · 2024Article
- Single-cell RNA sequencing reveals the differentiation and regulation of endplate cells in human intervertebral disc degeneration.Scientific reports · 2024Article
- Bromodomain inhibition targeting BPTF in the treatment of melanoma and other solid tumors.Clinical & experimental metastasis · 2024Review
- CCAT1 lncRNA is chromatin-retained and post-transcriptionally spliced.Histochemistry and cell biology · 2024Article
- Article
79 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
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon tumors arise in a stepwise fashion from either discrete genetic perturbations or epigenetic dysregulation. To uncover the key epigenetic regulators that drive colon cancer growth, we used a CRISPR loss-of-function screen and identified a number of essential genes, including the bromodomain and extraterminal (BET) protein BRD4. We found that BRD4 is critical for colon cancer proliferation, and its knockdown led to differentiation effects in vivo. JQ1, a BET inhibitor, preferentially reduced growth in a subset of epigenetically dysregulated colon cancers characterized by the CpG island methylator phenotype (CIMP). Integrated transcriptomic and genomic analyses defined a distinct superenhancer in CIMP+ colon cancers that regulates cMYC transcription. We found that the long noncoding RNA colon cancer-associated transcript 1 (CCAT1) is transcribed from this superenhancer and is exquisitely sensitive to BET inhibition. Concordantly, cMYC transcription and cell growth were tightly correlated with the presence of CCAT1 RNA in a variety of tumor types. Taken together, we propose that CCAT1 is a clinically tractable biomarker for identifying patients who are likely to benefit from BET inhibitors.
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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.