ArticleTranslational cancer research2026
YTHDF1 enhances ACSL3 translation in an m6A-dependent manner to regulate lipid metabolism and colorectal cancer progression.
Article in Translational cancer research, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: While N Methods: The Cancer Genome Atlas-READ database was used to compare the expression levels of YTHDF1 and ACSL3 in READ and normal tissues. Lentivirus-mediated knockdown and overexpression of YTHDF1 and ACSL3 were performed in the human READ cell line SW1463. Cellular phenotypes were evaluated through Cell Counting Kit-8 viability assays, colony formation and proliferation assays, flow cytometric cell cycle and apoptosis analyses, wound healing migration tests, and Transwell invasion experiments. Intracellular concentrations of cholesterol, triglycerides, and adenosine triphosphate were quantified with commercial assay kits. Molecular interactions between YTHDF1 and ACSL3 were examined using RNA immunoprecipitation, crosslinking immunoprecipitation, m Results: YTHDF1 was significantly upregulated in READ tissues. Its knockdown suppressed proliferative, migratory, invasive, and lipid synthetic activities in READ cells. ACSL3 was confirmed as a functional target of YTHDF1 bearing m Conclusions: YTHDF1 enhances ACSL3 translation in an m
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.