ReviewClinical and translational medicine2026
Lactylation in colorectal cancer: Unveiling novel mechanisms in metabolism, progression and therapeutic targeting.
Review in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- circZNF148 Drives Glucose Metabolism Reprogramming to Enhance Metastasis and Immune Evasion via HK1 Stabilization in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lactylation in colorectal cancer: Unveiling novel mechanisms in metabolism, progression and therapeutic targeting.Clinical and translational medicine · 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
7 authors.
Funding
Abstract
backgroundColorectal cancer is a leading cause of cancer mortality characterised by a unique metabolic microenvironment and complex interactions with the gut microbiota. Lactylation, a novel post-translational modification derived from lactate, has emerged as a key epigenetic regulator connecting metabolic reprogramming to gene expression. While its general roles in cancer are recognised, the tissue-specific regulatory network of lactylation in colorectal cancer-particularly its interplay with the gut microbiome and specific chemotherapy resistance mechanisms-remains underexplored. MAIN BODY: This review systematically dissects the dynamic 'writer‒eraser‒reader' network of lactylation, highlighting its distinct oncogenic functions in colorectal cancer. We reveal a critical 'microbiome‒metabolism‒epigenetics' axis in which gut flora-derived metabolites (including D-lactate) remodel the tumour microenvironment and drive immune evasion. Beyond histone modifications, we emphasise the pivotal role of non-histone lactylation targets (e.g., eEF1A2, PD-L1) in orchestrating malignant proliferation and promoting liver metastasis by priming the pre-metastatic niche. Furthermore, we elucidate novel mechanisms by which lactylation induces resistance to standard chemotherapeutic agents (5-fluorouracil and oxaliplatin), specifically through the enhancement of DNA repair and the suppression of ferroptosis. We also critically evaluate the pharmacological challenges hindering clinical translation, such as the poor selectivity of current broad-spectrum inhibitors. SHORT
conclusionLactylation serves as a fundamental metabolic‒epigenetic link driving aggressive phenotypes in colorectal cancer. By delineating these tissue-specific mechanisms and proposing next-generation site-specific targeting strategies, this review provides a theoretical foundation for developing precision medicine interventions to overcome therapy resistance in colorectal cancer patients.
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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 Socratic graph.