ArticleEBioMedicine2026
The AGPS regulatory variant rs113671272 confers esophageal squamous cell carcinoma susceptibility through allele-specific MEIS3 binding and NF-κB activation in Chinese populations.
Article in EBioMedicine, 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
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal squamous cell carcinoma (ESCC) demonstrates pronounced ethnic disparities, being prevalent in Asian populations. However, the genetic mechanisms underlying this disparity remain poorly understood. This study aims to characterise the functional contribution of the regulatory variant rs113671272 in alkylglycerone phosphate synthase (AGPS) to ESCC susceptibility and prognosis in Chinese cohorts.
methodsWe conducted a two-phase genome-wide association study (GWAS) comprising 6172 participants to identify risk loci. Functional validation was conducted through Cleavage Under Targets & Tagmentation-quantitative PCR (CUT&Tag-qPCR) assay, Electrophoretic mobility shift assay (EMSA), and analyses of clinically annotated specimens with confirmed genotypes. In vitro and in vivo models, including RNA interference, and xenograft tumours, were employed to assess phenotypic effects. Transcriptomic profiling and Western blotting elucidated downstream pathways. Clinical correlations were evaluated in multi-ethnic cohorts.
findingsAGPS 5'UTR regulatory variant rs113671272 was identified as a susceptibility locus for ESCC (OR = 1.15, P = 0.0004), with the A allele conferring poor survival. This variant localises to a putative active regulatory element marked by H3K27ac/H3K4me1/H3K4me3 and exhibits allele-specific binding to the transcription factor MEIS3. The co-expression of AGPS and myeloid ecotropic viral integration site 3 (MEIS3) was significantly associated with worse survival in Chinese, but not Caucasian patients with ESCC. MEIS3 knockdown significantly suppressed AGPS expression. AGPS knockdown inhibited ESCC cell proliferation, migration, and tumour growth, whereas its overexpression promoted oncogenic phenotypes via NF-κB activation. MEIS3 knockdown suppressed ESCC cell proliferation and migration, consistent with a pro-oncogenic role similar to that of AGPS.
interpretationOur results establish rs113671272 as a key ethnic-specific ESCC risk variant that operates through the MEIS3/AGPS/NF-κB regulatory axis. These findings provide mechanistic insights into population disparities in ESCC and highlight the potential of AGPS-targeted strategies for risk assessment and precision therapy in high-risk populations.
fundingNational Natural Science Foundation of China U22A20326.
Indexed as
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.