ArticleExperimental cell research2026
S-nitrosylated COX-2 is a microenvironment-regulated breast cancer cell biomarker of mesenchymal phenotypes.
Article in Experimental cell research, 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
- Update of
Authors and funding
7 authors.
Funding
Abstract
COX-2, an inducible enzyme key to production of inflammatory prostaglandins, has tumor cell-intrinsic oncogenic activity. Previously, we reported Cys-526-nitrosylated COX-2 (SNO-COX-2) associates with breast cancer progression and poor-prognostic young onset breast cancer. Here, using a 3D culture model of early-stage human breast cancer (MCF10DCIS cells), we report SNO-COX-2, but not non-nitrosylated COX-2, closely associated with mesenchymal cell phenotypes induced by fibrillar Col1. Inhibition of nitric oxide synthase (NOS) activity did not reduce SNO-COX-2 levels, suggesting alternative nitrosylation mechanisms. In 3D MCF10DCIS culture, mesenchymal phenotypes and SNO-COX-2 protein induced by Col1 did not associate with transcription of classic epithelial-to-mesenchymal transition (EMT) markers nor common cancer signaling pathways. Conversely, TGFβ-1 strongly induced EMT- and cancer signaling-related transcripts but was insufficient to increase SNO-COX-2 protein or mesenchymal phenotypes. These data suggest the mesenchymal phenotype and SNO-COX-2 expression in MCF10DCIS are driven by a non-transcriptional mechanism dependent on Col1. We tested 300 additional microenvironmental conditions and find SNO-COX-2 expression is driven by inflammatory, wound-resolving, and cancer-associated TME factors, including TNC, SPP1, decorin, Col1, Col3, INF-γ, and IL-4/13, with specific extracellular matrix-ligand combinations driving both high and low SNO-COX-2 expression. In sum, these observations show that in MCF10DCIS cells, SNO-COX-2 associates with mesenchymal phenotypes more strongly than non-nitrosylated COX-2; expression of classic EMT transcripts is neither sufficient nor necessary for acquisition of mesenchymal phenotypes; and expression of SNO-COX-2 is highly microenvironment-dependent. Future studies evaluating SNO-COX-2 as a biomarker for early-stage breast cancer with increased risk for progression, and its regulation, are warranted.
Indexed as
Identifiers
What 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.