ArticleMolecular biology reports2026
Tumor-derived ITGB3 shapes a primed but functionally constrained NK cell state in breast cancer through HLA-E-NKG2A signaling.
Article in Molecular biology reports, 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
backgroundNatural killer (NK) cells are vital for anti-tumor immunity, yet their effector functions are frequently constrained within the tumor microenvironment. Integrin β3 (ITGB3) has been implicated in breast cancer progression and stemness, but whether ITGB3 expression in malignant cells influences NK cell states and contributes to immune evasion remains unclear.
methodsSingle-cell RNA sequencing data were utilized to profile the transcriptomic and metabolic divergence of NK cells between ITGB3⁺ and ITGB3⁻ tumor microenvironments. Cell-cell communication and pseudotime trajectory analyses were performed to identify key signaling axes. The SCIPAC framework was employed to map single-cell subsets to the bulk TCGA-BRCA cohort for clinical correlation. The mechanistic findings were validated through in vitro co-culture assays and NKG2A blocking experiments using MDA-MB-231 and BT-474 cell lines.
resultsNK cells associated with ITGB3
conclusionsITGB3 expression in malignant cells is associated with a primed but functionally constrained NK cell state in breast cancer. Increased malignant-cell HLA-E expression and restoration of IFN-γ production following NKG2A blockade support a functional contribution of the inhibitory NKG2A branch, without excluding concurrent activating signaling through NKG2C.
Indexed as
Identifiers
42507293What 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.