ReviewMedComm2026
Protein Lactylation in Cancer: Mechanisms and Therapeutic Targets.
Review in MedComm, 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
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
2 citing papers in PubMed.
- Lactate-Induced ZMYM2 K529 Lactylation Stabilizes ZMYM2 and Promotes Platinum Resistance in Ovarian Cancer.International journal of molecular sciences · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Warburg effect states that cancer cells preferentially undergo aerobic glycolysis, producing lactate as a key metabolic byproduct. Lactate acidifies the tumor microenvironment (TME) and serves as a signaling molecule and substrate for lysine lactylation (Kla), a novel posttranslational modification (PTM) discovered in 2019 that links glycolytic metabolism to epigenetic and proteomic reprogramming. The reversible modification of histones and nonhistone proteins orchestrates oncogenic adaptation and drives tumor progression. However, gaps persist in our understanding of the multifactorial regulation of lactylation and its translational potential in overcoming tumor heterogeneity and resistance. This review highlights the emerging roles of lactylation in cancer therapies, including the enhancement of DNA repair mechanisms during chemotherapy, stabilization of key signaling effectors upon targeted therapy, and promotion of an immunosuppressive TME in immunotherapy. We further examined regulatory factors associated with lactylation, from competitive PTMs and genetic mutations to microbial influences and environmental signals. Additionally, we discuss the therapeutic potential of targeting lactylation via indirect modulators currently under investigation and the visualization of lactate and lactylation modifications. By synthesizing these insights, this review highlights lactylation as a reversible metabolic-epigenetic axis for precision oncology, enabling predictive biomarkers, combination strategies, and novel interventions to address the dynamic challenges of 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.