ReviewMolecular medicine reports2025
Impact of lactylation on the pathogenesis of cancer and its clinical application potential (Review).
Review in Molecular medicine reports, 2025. 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.
- Lactylation and targeted therapy resistance in hepatocellular carcinoma.Clinical epigenetics · 2026Review
- Lactylation in digestive system tumors: from mechanisms to therapeutic target.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of lactate metabolism is a hallmark of multiple pathologies, including cancer, which coordinates metabolic reprogramming and malignant progression. Lactylation, a lactate‑derived post‑translational modification, is a key regulator of tumor cell adaptation, aggressive behavior and immune escape. This modification mechanism links lactate accumulation to carcinogenic signaling and epigenetic dysregulation, providing novel insights into cancer pathogenesis. The present review summarizes the roles of lactylation in tumor microenvironment (TME) remodeling, therapeutic resistance and immunomodulation, and outlines the challenges to clinical translation. Lactate drives the lactylation of histone and non‑histone proteins, and alters chromatin structure and transcriptional programs to maintain tumorigenesis. In the TME, lactylation modulates the phenotypes of stromal cells (such as cancer‑associated fibroblasts) and immune cells (including macrophages and T cells), forming an immunosuppressive niche. Lactylation can also polarize macrophages towards a tumor‑promoting state, inhibit CD8+ T cells and upregulate immune checkpoints. Clinically, lactylation is associated with chemotherapy resistance (such as paclitaxel in breast cancer) and a poor prognosis, highlighting its usefulness as a biomarker. Notably, therapeutic strategies targeting lactate synthesis (such as lactate dehydrogenase A inhibitors), lactate transport (for example, monocarboxylate transporter 1/4 blockers) or lactase (such as histone lactate transferase) have shown promise in preclinical models. In conclusion, lactylation promotes tumor progression while also providing a viable therapeutic target. Deciphering its environment‑dependent mechanisms, particularly its interactions with immune checkpoints and metabolic vulnerabilities, may advance precision oncology. Validating biomarkers and therapies centered on lactylation is a key frontier in improving clinical outcomes.
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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.