ArticleHuman cell2026
Extracellular vesicle-derived CDCP1 promotes chemoresistance and macrophage polarization in breast cancer.
Article in Human cell, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer derived extracellular vesicles (EVs) mediate tumor progression through surface protein-dependent intercellular communication; however, their molecular heterogeneity remains poorly characterized. In this study, we employed a proximity-dependent barcoding assay (PBA) together with patient-derived organoid (PDO) models and identified CDCP1 as a key driver of EV-mediated oncogenesis. PBA-based surface proteomics revealed CDCP1 as the most upregulated protein in breast cancer-derived EVs compared with EVs from normal tissues. Clinical validation confirmed elevated CDCP1 expression in tumor tissues and matched EVs. PDOs generated from fresh clinical specimens recapitulated CDCP1 expression levels of the parental tumors and secreted CDCP1-enriched EVs. Functional experiments showed that CDCP1-knockdown EVs suppressed PDO proliferation and sensitized tumors to chemotherapy. Mechanistically, CDCP1-positive EVs promoted macrophage polarization toward an M2 phenotype, accompanied by upregulation of IL-10 and TGF-β and CCL22. Multiplex immunofluorescence confirmed that CDCP1-high tumors exhibited increased co-localization of CD68⁺ and CD163⁺ macrophages. These results establish CDCP1 as a master regulator of EV driven breast cancer progression, linking surface proteome remodeling to chemo-resistance and immunosuppressive microenvironment reprogramming. The integration of single-EV profiling and PDO modeling establishes a translational framework for targeting CDCP1 as a promising therapeutic target and a candidate biomarker for future liquid biopsy development in aggressive breast cancer subtypes.
Indexed as
Identifiers
41975113What 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.