ArticleFood science & nutrition2020
Apigenin upregulation of CD26/DPPIV on colon epithelial cells requires inhibition of casein kinase 2.
Article in Food science & nutrition, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Filovirus infection disrupts epithelial barrier function and ion transport in human iPSC-derived gut organoids.PLoS pathogens · 2025Article
- Unveiling the power of flavonoids: A dynamic exploration of their impact on cancer through matrix metalloproteinases regulation.BioMedicine · 2024Review
- Apigenin directly interacts with and inhibits topoisomerase 1 to upregulate CD26/DPP4 on colorectal carcinoma cells.Frontiers in pharmacology · 2022Article
- Does Oral Apigenin Have Real Potential for a Therapeutic Effect in the Context of Human Gastrointestinal and Other Cancers?Frontiers in pharmacology · 2021Review
- Apigenin upregulation of CD26/DPPIV on colon epithelial cells requires inhibition of casein kinase 2.Food science & nutrition · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD26/DPPIV is a cell surface glycoprotein found on cells of the intestinal epithelium including those of the colon. We have previously shown that the dietary flavone apigenin (4',5,7-trihydroxyflavone) upregulates CD26/DPPIV on colon cells. Flavonoids such as apigenin interfere with the action of multiple cellular protein kinases and have the capacity to modulate the cell exterior and its ability to interface with the local environment through different signaling pathways. We show here that the ability of apigenin to upregulate CD26/DPPIV is exerted through and requires the activity of casein kinase 2 (CK2). Inhibitors of CK2 that are distinct from apigenin (emodin, 6-methyl-1,3,8-trihydroxyanthraquinone; TBB, 4,5,6,7-tetrabromobenzotriazole; and DRB, 5,6-dichlorobenzimidazole 1-β-D-ribofuranoside) showed a dose-dependent ability to increase CD26/DPPIV and had the same maximal effect when combined with apigenin at submaximal concentrations. Knockdown of CK2 with siRNA abrogated the ability of apigenin to upregulate CD26/DPPIV. Apigenin treatment of cells had no effect on the levels of CK2 protein, consistent with an inhibition of activity of the enzyme. Apigenin's upregulation of CD26/DPPIV in differentiated human colon epithelial cells depends upon inhibition of CK2 activity. This is a key step in enabling apigenin's ability to regulate the functions of intestinal epithelial cells.
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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.