ArticleJournal of translational medicine2026
Fusobacterium nucleatum promotes tumor progression driven by histone lactylation through increasing GLUT1 expression in colorectal cancer.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- From Symbiont to Potential Carcinogenic Contributor: Examining the Pathogenic Evolution ofInfection and drug resistance · 2026Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe gut microbiota plays a significant role in the incidence and progression of colorectal cancer(CRC), with Fusobacterium nucleatum (F. nucleatum) identified as a contributor to the advancement of this malignancy. However, the precise mechanisms underlying its action remain unclear.
methodsThis study uses FISH technology to measure F. nucleatum in tumors and WB to examine histone lactylation, exploring their connection. HCT116 CRC cells were treated with lactic acid, Oxamate, 2-DG, and F. nucleatum supernatant to analyze histone lactylation and cell behaviors like proliferation, migration, and invasion. The research also screened F. nucleatum supernatant for compounds that increase tumor cell lactylation and assessed their effects on cell viability using CCK-8, EdU, and transwell assays. Additionally, GLUT agonists and inhibitors were used to demonstrate that formic acid in the supernatant elevates GLUT1 expression.
resultsTumors characterized by elevated nuclear levels demonstrate increased histone lactylation. Modulating histone lactylation levels in tumor cells through human intervention can substantially impact their proliferative, migratory, and invasive capacities. Our study identified that F. nucleatum enhances the expression of GLUT1 in tumor cells via its metabolite, formic acid, leading to increased lactate production and histone lactylation. This process ultimately augments the stemness of tumor cells.
conclusionsF. nucleatum enhances the expression of GLUT1 in colorectal cancer cells through the production of formic acid, which subsequently elevates histone lactate levels and facilitates tumor progression.
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.