ArticleApoptosis : an international journal on programmed cell death2026
The histone demethylase KDM4A promotes esophageal cancer progression by epigenetically activating LRG1-mediated TGF-β signaling.
Article in Apoptosis : an international journal on programmed cell death, 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.
- The role of OTUD1-mediated deubiquitination in disease pathogenesis: from molecular mechanisms to clinical translation.Frontiers in immunology · 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
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) remains a lethal malignancy with a poor 5-year survival rate of approximately 20%, necessitating the identification of novel therapeutic targets. Here, we show that KDM4A is significantly upregulated in esophageal squamous cell carcinoma (ESCC) and its high expression correlates with poor prognosis. Functional assays demonstrated that KDM4A promotes ESCC cell proliferation, migration, invasion, and tumor growth in vitro and in vivo. Mechanistically, KDM4A demethylates H3K9me3 at the LRG1 promoter, thereby enhancing LRG1 transcription and activating the TGF-β pathway to drive epithelial-mesenchymal transition (EMT) and cancer stemness. Knockdown of KDM4A or LRG1 suppresses these oncogenic phenotypes, while LRG1 overexpression rescues KDM4A deficiency-induced impairments. Clinically, KDM4A and LRG1 are co-overexpressed in ESCC tissues and associated with advanced tumor stage and shorter overall survival. These findings identify the KDM4A-LRG1-TGF-β axis as a critical driver of ESCC progression and a potential therapeutic target.
Indexed as
Identifiers
41811529What OpenQuestion 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 OpenQuestion graph.