ReviewCells2025
"Unraveling EMILIN-1: A Multifunctional ECM Protein with Tumor-Suppressive Roles" Mechanistic Insights into Cancer Protection Through Signaling Modulation and Lymphangiogenesis Control.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- Loss of EMILIN-1/integrin axis drives microenvironmental reprogramming in gastric tumorigenesis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Article
- Integrative Proteomics of Extracellular Vesicles from hiPSC-Derived Cardiac Organoids Reveals Heart Tissue-like Molecular Representativity.International journal of molecular sciences · 2026Article
- Roles and molecular mechanisms of EMILIN-1 in physiology and disease: a narrative review.Frontiers in medicine · 2026Review
- EMILIN-1 in the tumor microenvironment: insights from CNS tumors and beyond.Frontiers in oncology · 2026Review
- Beyond COL1A1::PDGFB: Rare fusions and their clinical implications in dermatofibrosarcoma protuberans.World journal of clinical cases · 2025Article
- Heterogeneity of Extracellular Vesicles and Non-Vesicular Nanoparticles in Glioblastoma.Journal of extracellular vesicles · 2025Article
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
Abstract
EMILIN-1 (Elastin Microfibril Interface Located Protein 1) is an extracellular matrix homotrimeric glycoprotein belonging to the EMILIN/Multimerin family, with both structural and regulatory roles, increasingly recognized for its tumor-suppressive functions. Initially identified for its involvement in elastogenesis and vascular homeostasis, EMILIN-1 has gradually emerged as a key player in cancer biology. It exerts its anti-tumor activity through both direct and indirect mechanisms: by regulating tumor cell proliferation and survival and by modulating lymphangiogenesis and the associated inflammatory microenvironment. At the molecular level, EMILIN-1 inhibits pro-oncogenic signaling pathways, such as ERK/AKT and TGF-β, via its selective interaction with α4/α9 integrins. In the tumor microenvironment, it contributes to tissue homeostasis by restraining aberrant lymphatic vessel formation, a process closely linked to tumor dissemination and immune modulation. Notably, EMILIN-1 expression is frequently reduced or its structure altered by proteolytic degradation in advanced cancers, correlating with disease progression and poor prognosis. This review summarizes the current knowledge on EMILIN-1 in cancer, focusing on its dual function as an active extracellular matrix regulator of intercellular signaling. Particular attention is given to its mechanistic role in the control of cell proliferation, underscoring its potential as a novel biomarker and therapeutic target in oncology.
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.