ArticleOncology letters2012
Chemically modified heparins inhibit fibrinogen-bridged indirect adhesion between tumor cells and platelets.
Article in Oncology letters, 2012. 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
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Platelet-derived extracellular vesicles inhibit ferroptosis and promote distant metastasis of nasopharyngeal carcinoma by upregulating ITGB3.International journal of biological sciences · 2022Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction between platelets and tumor cells is critical for the hematogenous metastasis of tumor cells. We recently reported that fibrinogen was capable of bridging and enhancing the interaction of platelets and tumor cells under conditions of physical shear force. In the present study, we aimed to detect the effects of 8 chemically modified heparins on the binding of fibrinogen to platelets or tumor cells using flow cytometry assays, as well as the fibrinogen-bridged adhesion of platelets and tumor cells using flow chamber assays. The results showed that fibrinogen binds to platelets and tumor cells in a β3 integrin-dependent manner and bridges the adhesion between platelets and tumor cells. Heparin and certain chemically modified heparins, including borohydride-reduced (RO)-, carboxyl-reduced (CR)- and 2-O, 3-O-desulfated (2/3ODS)-heparins, inhibited the β3 integrin-dependent adhesion of fibrinogen to platelets or tumor cells, and consequently blocked the fibrinogen-bridged indirect adhesion of platelets to tumor cells. These data indicate that chemically modified heparins should be potential inhibitors for the fibrinogen-bridged indirect adhesion of platelets and tumor cells, which provides a novel explanation of the anti-adhesion property of heparin and proposes a new anti-metastatic target for cancer treatment.
Identifiers
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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.