Evidence map›Paper›PMID 28337019›Full record

ArticleScientific reports2017

Apigenin-induced lysosomal degradation of β-catenin in Wnt/β-catenin signaling.

Chung-Ming Lin, Hsin-Han Chen, Chun-An Lin, Hui-Chung Wu, Jim Jinn-Chyuan Sheu, Hui-Jye Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 64 citations in OpenAlex.

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  14. Natural Polyphenols for Treatment of Colorectal Cancer.Molecules (Basel, Switzerland) · 2022
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  20. PARP-1-Associated Pathological Processes: Inhibition by Natural Polyphenols.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Chung-Ming LinDepartment of Biotechnology, Ming-Chuan University, Taoyuan, 33348, Taiwan.
Hsin-Han ChenDivision of Plastic and Reconstructive Surgery, Department of Surgery, China Medical University Hospital, Taichung, 40402, Taiwan.
Chun-An LinGraduate Institute of Basic Medical Science, China Medical University, Taichung, 40402, Taiwan.
Hui-Chung WuDepartment of Biotechnology, Ming-Chuan University, Taoyuan, 33348, Taiwan.
Jim Jinn-Chyuan SheuInstitute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung, 80424, Taiwan.
Hui-Jye ChenGraduate Institute of Basic Medical Science, China Medical University, Taichung, 40402, Taiwan. huijyechen@mail.cmu.edu.tw.
Ming Chuan University · TWChina Medical University · TWChina Medical University Hospital · TWNational Sun Yat-sen University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The bioflavonoid apigenin has been shown to possess cancer-preventive and anti-cancer activities. In a drug screening, we found that apigenin can inhibit Wnt/β-catenin signaling, a pathway that participates in pivotal biological functions, which dis-regulation results in various human diseases including cancers. However, the underlying mechanism of apigenin in this pathway and its link to anti-cancer activities remain largely unknown. Here we showed that apigenin reduced the amount of total, cytoplasmic, and nuclear β-catenin, leading to the suppression in the β-catenin/TCF-mediated transcriptional activity, the expression of Wnt target genes, and cell proliferation of Wnt-stimulated P19 cells and Wnt-driven colorectal cancer cells. Western blotting and immunofluorescent staining analyses further revealed that apigenin could induce autophagy-mediated down-regulation of β-catenin in treated cells. Treatment with autophagy inhibitors wortmannin and chloroquine compromised this effect, substantiating the involvement of autophagy-lysosomal system on the degradation of β-catenin during Wnt signaling through inhibition of the AKT/mTOR signaling pathway. Our data not only pointed out a route for the inhibition of canonical Wnt signaling through the induction of autophagy-lysosomal degradation of key player β-catenin, but also suggested that apigenin or other treatments which can initiate this degradation event are potentially used for the therapy of Wnt-related diseases including cancers.

Indexed as

AutophagyWnt Signaling PathwayApigeninbeta CateninCell Line, TumorCell ProliferationColorectal NeoplasmsDishevelled ProteinsHumansLow Density Lipoprotein Receptor-Related Protein-5LysosomesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesApigeninbeta CateninCTNNB1 protein, humanDishevelled ProteinsLow Density Lipoprotein Receptor-Related Protein-5LRP5 protein, humanMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID28337019
PMCPMC5428476
OpenAlexW2595834232

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.