ReviewJournal of gastrointestinal oncology2026
MNAT1 in gastrointestinal cancers: mechanistic insights and therapeutic strategies-a narrative review.
Review in Journal of gastrointestinal oncology, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objective: Ménage à trois 1 (MNAT1) is an essential scaffolding subunit of the cyclin-dependent kinase (CDK)-activating kinase (CAK) complex and has been increasingly implicated in cancer pathogenesis. Given the accumulating evidence linking MNAT1 to gastrointestinal (GI) malignancies, this narrative review aims to summarize current knowledge regarding the biological functions, oncogenic roles and therapeutic potential of MNAT1 in GI cancers. Methods: A literature search of the relevant databases (PubMed, Web of Science) was conducted, with a focus on recent and key publications in the English language. The search strategy included terms related to MNAT1, GI cancer, CAK complex and therapeutic targeting. Key Content and Findings: MNAT1 stabilizes the CAK complex and promotes cell-cycle progression by enabling CAK-mediated T-loop phosphorylation of cell-cycle CDKs. In addition, CAK functions as a module of the general transcription factor II H (TFIIH) and supports phosphorylation of RNA polymerase II (Pol II) at active promoters, sustaining oncogenic transcription programs. Therapeutic strategies that target MNAT1/CAK include CDK7 inhibition and CAK complex degradation, both of which can suppress transcriptional output and induce cell-cycle arrest. Combination regimens incorporating MNAT1/CAK targeting have also shown preclinical efficacy. Conclusions: This review summarizes current evidence on MNAT1 across multiple malignancies, with a focus on gastrointestinal cancers. We discuss MNAT1 as a potential biomarker for prognosis and treatment response and highlight opportunities and challenges for therapeutically targeting MNAT1/CAK in gastrointestinal cancer.
Indexed as
Identifiers
What Socratic 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 Socratic graph.