ArticleScientific reports2017
Integrin β3/Akt signaling contributes to platelet-induced hemangioendothelioma growth.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 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
7 citing papers in PubMed, 12 citations in OpenAlex.
- Tumor-platelet cross talk in cancer: mechanisms, thrombotic risk, and translational opportunities.Blood advances · 2026Review
- Platelets in cancer and immunotherapy: functional dynamics and therapeutic opportunities.Experimental hematology & oncology · 2025Review
- Pan-cancer analysis of ITGB3 as a potential prognostic and immunological biomarker.Discover oncology · 2025Article
- CBX7 is involved in the progression of cervical cancer through the ITGβ3/TGFβ1/AKT pathway.Oncology letters · 2024Article
- The dynamic role of platelets in cancer progression and their therapeutic implications.Nature reviews. Cancer · 2024Review
- ITGB3/CD61: a hub modulator and target in the tumor microenvironment.American journal of translational research · 2019Review
- MicroRNA let-7a regulates angiogenesis by targeting TGFBR3 mRNA.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemangioendothelioma (HE) is a type of angiomatous lesions that features endothelial cell proliferation. Understanding the mechanisms orchestrating HE angiogenesis can provide therapeutic insights. It has been shown that platelets can support normal and malignant endothelial cells during angiogenesis. Using the mouse endothelial-derived EOMA cell line as a model of HE, we explored the regulatory effect of platelets. We found that platelets stimulated EOMA proliferation but did not mitigate apoptosis. Furthermore, direct platelet-EOMA cell contact was required and the proliferation was mediated via integrin β3/Akt signaling in EOMA cells. SiRNA knockdown of integrin β3 and inhibition of Akt activity significantly abolished platelet-induced EOMA cell proliferation in vitro and tumor development in vivo. These results provide a new mechanism by which platelets support HE progression and suggest integrin β3 as a potential target to treat HE.
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.