ReviewBiomarker research2026
Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.
Review in Biomarker 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
7 authors.
Funding
Abstract
Post-translational modifications (PTMs) of histone H3 at lysine 9 (H3K9) contribute to chromatin homeostasis and transcriptional regulation and have been implicated in cancer progression. However, how distinct H3K9 modification states differ in function, compete for the same lysine residue, and dynamically respond to cellular context remains incompletely understood. This review summarizes the biochemical characteristics and enzymatic regulation of H3K9 methylation, acetylation, and non-acetyl acylations, including lactylation, β-hydroxybutyrylation, butyrylation, and crotonylation. We examine their roles in DNA replication, transcription, and DNA damage repair, as well as their interplay with other epigenetic regulatory mechanisms. We further discuss how H3K9-associated regulatory networks contribute to tumor proliferation, stemness maintenance, metabolic reprogramming, invasion and metastasis, immune microenvironment remodeling, therapeutic resistance, and programmed cell death, emphasizing their context-dependent and, in some settings, opposing biological effects. Finally, we evaluate preclinical and clinical advances in pharmacologically targeting H3K9-associated regulatory enzymes, distinguishing residue-specific mechanistic evidence from broader enzyme-level effects, and outline future directions for biomarker-guided epigenetic therapies in cancer.
Indexed as
Identifiers
42888460What 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.