ArticleJournal of molecular histology2026
NR2C2 suppresses breast cancer progression and promotes T-Cell infiltration in the tumor microenvironment.
Article in Journal of molecular histology, 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
Members of the nuclear receptor subfamily 2, group C (NR2Cs), despite sharing structural homology with established biomarkers like estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), remain underexplored in breast cancer (BC). This study aims to elucidate the subtype-specific prognostic significance of NR2Cs and investigate the molecular and immunomodulatory mechanisms of NR2C2 in restricting BC progression. We integrated transcriptomic data from TCGA with functional genomics to analyze NR2Cs expression and patient prognosis. Mechanistic landscapes were characterized using pathway enrichment, protein-protein interaction networks, immune infiltration algorithms, and pharmacogenomic drug sensitivity correlation. In vitro validation was performed using cell proliferation, colony formation, 5-Ethynyl-2'-deoxyuridine (EdU), and wound healing assays. In vivo antitumor efficacy and T-cell infiltration levels were evaluated using orthotopic human MDA-MB-231 xenografts in BALB/c nude mice and syngeneic murine EO771 tumors in immunocompetent C57BL/6 mice, supplemented by multiplexed immunohistochemistry. Both NR2C1 and NR2C2 were significantly downregulated in BC tissues compared with normal controls. NR2C2 demonstrated a robust, pan-subtype protective profile, correlating with prolonged survival across major molecular subtypes, particularly in ER-positive cohorts. In silico profiling connected NR2C2 to transforming growth factor-β (TGF-β) pathway inhibition and tumor-immune T-cell infiltration enhancement. In vitro, NR2C2 overexpression significantly suppressed BC cell proliferation, colony formation, DNA synthesis, and migratory capabilities. In vivo, NR2C2 overexpression markedly restricted tumor growth in both models. Mechanistically, this tumor-suppressive effect was characterized by cell-intrinsic growth arrest (decreased Ki-67), induced apoptosis (increased Cleaved Caspase-3), and significant inhibition of the TGF-β pathway (decreased Smad). Concurrently, in the immunocompetent syngeneic model, Nr2c2 overexpression promoted a robust recruitment of infiltrating CD4
Indexed as
Identifiers
42828550What 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.