Evidence map›Paper›PMID 27390525›Full record

ArticleOncoTargets and therapy2016

Downregulation of human Wnt3 in gastric cancer suppresses cell proliferation and induces apoptosis.

Hai-Sheng Wang, Xiaobo Nie, Rui-Bing Wu, Hong-Wei Yuan, Yue-Hong Ma, Xiu-Lan Liu, Jian-Yu Zhang, Xiu-Ling Deng, Qin Na, Hai-Yan Jin and 4 more

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

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  3. Unleashing Wnts: Wnt Ligands Fuel Cancer Spread.Journal of cancer biology · 2025
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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

14 authors at 1 institution in 1 country.

Hai-Sheng WangKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Xiaobo NieKey Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University, Kaifeng.
Rui-Bing WuKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Hong-Wei YuanKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Yue-Hong MaKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Xiu-Lan LiuKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Jian-Yu ZhangKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Xiu-Ling DengKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Qin NaKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Hai-Yan JinKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Yan-Chao BianKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot.
Yu-Min GaoEpidemiology Section, Public Health School, Inner Mongolia Medical University, Hohhot.
Yan-Dong WangState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, People's Republic of China.
Wei-Dong ChenKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University, Hohhot; Key Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University, Kaifeng.
Beijing University of Chemical Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant activation of Wnt/β-catenin signaling pathways is closely involved in the occurrence and progression of several types of human malignancies. However, as a fundamental component in this cascade, Wnt3 has not been well understood for the expression level and pathogenic mechanism in gastric carcinogenesis. Here, this research was undertaken to elucidate the important role of Wnt3 in gastric cancer. Wnt3 expression in gastric carcinomas and their respective normal tissues was examined by immunoblotting and immunohistochemistry. In all cases, Wnt3 expression was significantly elevated in gastric carcinomas compared with normal tissues. Knocking down Wnt3 in MGC-803 gastric cancer cells by small interfering RNAs transfection led to an obvious decrease in both transcript and protein levels. Silence of Wnt3 expression in gastric cancer cells inhibited the expression of β-catenin and cyclin D1 genes in Wnt/β-catenin pathway, significantly blocked cellular proliferation, delayed cell cycle, suppressed cell invasion and metastasis, accompanied by a higher apoptosis rate. Together, we conclude that upregulation of Wnt3 plays a crucial role in gastric tumorigenesis by inducing proliferation, migration, and invasion and inhibiting apoptosis of cancer cells, and Wnt3 might be a potential target for the treatment of gastric cancer.

Indexed as

gastric carcinogenesisgastric carcinomainvasionsiRNAβ-catenin

Identifiers

PMID27390525
PMCPMC4930241
OpenAlexW2461803522

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.