ArticleJournal of extracellular vesicles2026
Small Extracellular Vesicle-Derived Nidogen 1 Promotes HCC Carcinogenesis via Transglutaminase 3-Mediated YAP/TAZ Signalling.
Article in Journal of extracellular vesicles, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Nidogen 1-enriched extracellular vesicles drive HCC progression by inducing mregDC differentiation and Treg infiltration.Extracellular vesicles and circulating nucleic acids · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Tumour-derived small extracellular vesicles (sEV) are increasingly recognized as key mediators of cancer progression and metastasis by facilitating intercellular communication. In this study, we identify nidogen 1 (NID1), a basement membrane glycoprotein, as significantly enriched in sEV from metastatic hepatocellular carcinoma (HCC) cells. We demonstrate that the sEV-mediated delivery of NID1 enhances oncogenic behaviours, including proliferation, invasion and metastasis. Knockout mice of NID1 exhibited a marked delay in liver tumour formation induced by N-diethylnitrosamine (DEN) and carbon tetrachloride (CCL4), or hydrodynamic injection delivery of oncogenes, underscoring the role of NID1 in hepatocarcinogenesis. Importantly, we find that a stiffer extracellular matrix, a characteristic of tumour microenvironments, stimulates increased NID1 level in sEV. Using NID1 mutants, we identify the C-terminal domain as critical for its oncogenic functions, including promoting tumour growth and metastasis. Proteomic profiling reveals that transglutaminase 3 (TGM3) interacts with NID1 via its C-terminus. Subsequent analyses indicate that sEV-NID1 elevates TGM3 levels, leading to dysregulation of integrins and activation of the YAP/TAZ signalling pathway, thereby contributing to tumour progression. To explore therapeutic potential, we developed a novel monoclonal anti-NID1 antibody (anti-NID1 mAb) and evaluated its efficacy in multiple HCC mouse models. The antibody markedly suppressed liver tumour growth and metastasis of human and murine HCC cells. The therapeutic effect was further enhanced when combined with sorafenib, a standard treatment for HCC. Our findings delineate a novel sEV-NID1-TGM3 regulatory axis that promotes hepatocarcinogenesis and metastasis and suggest that targeting sEV-delivered NID1 with our homemade monoclonal antibody offers a promising avenue for therapeutic intervention in HCC.
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.