Evidence map›Paper›PMID 27507058›Full record

ArticleOncotarget2016

Chemoprevention of intestinal tumorigenesis by the natural dietary flavonoid myricetin in APCMin/+ mice.

Ye Li, Shu-Xiang Cui, Shi-Yue Sun, Wen-Na Shi, Zhi-Yu Song, Shu-Qing Wang, Xin-Feng Yu, Zu-Hua Gao, Xian-Jun Qu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

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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

9 authors at 1 institution in 2 countries.

Ye LiDepartment of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital Medical University, Beijing, China.
Shu-Xiang CuiBeijing Key Laboratory of Environmental Toxicology, Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing, China.
Shi-Yue SunDepartment of Pharmacology, Capital Medical University School of Basic Medical Sciences, Beijing, China.
Wen-Na ShiDepartment of Pharmacology, Capital Medical University School of Basic Medical Sciences, Beijing, China.
Zhi-Yu SongDepartment of Pharmacology, Capital Medical University School of Basic Medical Sciences, Beijing, China.
Shu-Qing WangDepartment of Pharmacology, Capital Medical University School of Basic Medical Sciences, Beijing, China.
Xin-Feng YuDepartment of Pharmacology, Capital Medical University School of Basic Medical Sciences, Beijing, China.
Zu-Hua GaoDepartment of Pathology, McGill University, Montreal, Quebec, Canada.
Xian-Jun QuDepartment of Pharmacology, Capital Medical University School of Basic Medical Sciences, Beijing, China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myricetin is a natural dietary flavonoid compound. We evaluated the efficacy of myricetin against intestinal tumorigenesis in adenomatous polyposis coli multiple intestinal neoplasia (APCMin/+) mice. Myricetin was given orally once a day for 12 consecutive weeks. APCMin/+ mice fed with myricetin developed fewer and smaller polyps without any adverse effects. Histopathological analysis showed a decreased number of dysplastic cells and degree of dysplasia in each polyp. Immunohistochemical and western blot analysis revealed that myricetin selectively inhibits cell proliferation and induces apoptosis in adenomatous polyps. The effects of myricetin were associated with a modulation the GSK-3β and Wnt/β-catenin pathways. ELISA analysis showed a reduced concentration of pro-inflammatory cytokines IL-6 and PGE2 in blood, which were elevated in APCMin/+ mice. The effect of myricetin treatment was more prominent in the adenomatous polyps originating in the colon. Further studies showed that myricetin downregulates the phosphorylated p38 MAPK/Akt/mTOR signaling pathways, which may be the mechanisms for the inhibition of adenomatous polyps by myricetin. Taken together, our data show that myricetin inhibits intestinal tumorigenesis through a collection of biological activities. Given these results, we suggest that myricetin could be used preventatively to reduce the risk of developing colon cancers.

Indexed as

Adenomatous Polyposis ColiAdenomatous Polyposis Coli ProteinAnimalsAntineoplastic AgentsCarcinogenesisChrysobalanaceaeDinoprostoneFlavonoidsGlycogen Synthase Kinase 3 betaHumansInterleukin-6Intestinal NeoplasmsMaleMiceMice, Inbred C57BLMice, Mutant StrainsAdenomatous Polyposis Coli ProteinAntineoplastic AgentsDinoprostoneFlavonoidsGlycogen Synthase Kinase 3 betaInterleukin-6MTOR protein, humanmyricetinTOR Serine-Threonine KinasesAPCMin/+ mouse modelchronic inflammationintestinal adenomatous polypsmyricetinWnt/β-catenin pathway

Identifiers

PMID27507058
PMCPMC5312395
OpenAlexW2476563968

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.