ArticleFEBS open bio2020
The rapid endocytic uptake of fetuin-A by adherent tumor cells is mediated by Toll-like receptor 4 (TLR4).
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Inter-organ crosstalk in systemic inflammation: a narrative review of molecular mechanisms and pharmacological modulation in the muscle-adipose-liver axis.Frontiers in pharmacology · 2026Review
- Fetuin-A Modulates Tumor Growth and Invasion in a Basal-like Triple Negative Breast Cancer Cell line, MDA-MB-468.Journal of pharmacy and pharmacology research · 2025Article
- The Role of Fetuin-A in Tumor Cell Growth, Prognosis, and Dissemination.International journal of molecular sciences · 2024Review
- Toll-like receptors in health and disease.MedComm · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Fetuin-A is a serum glycoprotein synthesized and secreted into blood by the liver and whose main physiological function is the inhibition of ectopic calcification. However, a number of studies have demonstrated that it is a multifunctional protein. For example, endocytic uptake of fetuin-A by tumor cells resulting in rapid cellular adhesion and spreading has been reported. The precise uptake mechanism, however, has been elusive. The present studies were done to determine whether Toll-like receptor-4 (TLR4), which has been previously shown to be a receptor for fetuin-A and is commonly expressed in immune cells, could take part in the rapid uptake (< 3 min) of fetuin-A by tumor cells. Rapid uptake of fetuin-A was inhibited by the specific TLR4 inhibitor CLI-095 and also attenuated in TLR4 knockdown prostate tumor cells. Inhibition of TLR4 by CLI-095 also attenuated the rapid adhesion of tumor cells as well as invasion through a bed of Matrigel. The data suggest mechanisms by which TLR4 modulates the adhesion and growth of tumor cells.
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Registered trials
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