ArticleNPJ precision oncology2026
HMGB3 facilitates malignant phenotype of esophageal carcinoma via histone lactylation- and Wnt/β-catenin-dependent transcription activation of c-myc.
Article in NPJ precision oncology, 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
9 authors.
Funding
Abstract
High-mobility group box 3 (HMGB3) mediates hypoxia-induced glycolysis in various cancers and acts as an oncogene in esophageal carcinoma (EC/ESCA). However, its roles in regulating glycolysis and histone lactylation during EC progression remain unclear. In this study, quantitative polymerase chain reaction (qPCR) and western blotting were conducted to measure HMGB3 levels in EC samples and cells. 5-Ethynyl-2'-deoxyuridine (EdU) assays, colony formation assays, and flow cytometry analyses were conducted to measure cell proliferation and apoptosis. Xenograft mouse models were established to explore tumorigenesis in vivo. Lactate production and glucose uptake were measured using commercial kits. Immunofluorescence staining was used to evaluate the co-localization of c-myc with lysine lactylation (Kla) and Ki67 expression in tumor tissue. A TOP/FOP assay was employed to evaluate Wnt/β-catenin pathway activity. Results revealed upregulated HMGB3 and elevated histone lactylation in EC. HMGB3 knockdown inhibited EC glycolysis, c-myc lactylation, and cell proliferation, yet promoted apoptosis, mimicking the effect of the glycolysis inhibitor 2-deoxy-D-glucose (2-DG). HMGB3 depletion also inactivated the Wnt/β-catenin signaling and impaired xenograft tumor growth, glycolysis, and lactylation. In conclusion, HMGB3 promotes EC malignant progression and tumor growth via histone lactylation and Wnt/β-catenin-mediated c-myc transcriptional activation.
Identifiers
What 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.