ArticleNature communications2026
A core transcriptional regulatory circuitry controls super-enhancer-driven activation of LGR5 in colorectal cancer.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
The core transcriptional regulatory program governed by a small set of master transcription factors is pivotal for establishing context-specific cellular features. Here, we report the roles of master factor MYC in actively regulating cancer-type specific super-enhancer activity and orchestrating a super-enhancer-dependent core transcriptional regulatory circuitry consisting of MYC, ETS2, and FOXP1 in colorectal cancer. The core regulatory module selectively promotes the transcription of super-enhancer-controlled genes in cooperation with co-activator BRD4, and perturbing the core circuitry factors sensitizes colon cancer cells to BET inhibition. LGR5, a key stemness gene, is activated in colorectal cancer at least in part by a circuitry-controlled distal super-enhancer, which is a frequently gained super-enhancer in colorectal cancer and required for metastasis propagation. These findings reveal a hierarchical transcription regulatory network in colorectal cancer, pinpoint distal enhancer as an important fuel for LGR5 overexpression in cancer, and provide insights for precisely targeting detrimental transcription events in therapy.
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.