Evidence map›Paper›PMID 29780251›Full record

ArticleOncoTargets and therapy2018

WWC3 inhibits epithelial-mesenchymal transition of lung cancer by activating Hippo-YAP signaling.

Qiang Han, Joachim Kremerskothen, Xuyong Lin, Xiupeng Zhang, Xuezhu Rong, Di Zhang, Enhua Wang

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In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  18. Frontiers in cell and developmental biology · 2020
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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

7 authors.

Qiang HanDepartment of Pathology, College of Basic Medical Sciences, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.
Joachim KremerskothenInternal Medicine D, Department of Nephrology, Hypertension and Rheumatology, University Hospital Muenster, Muenster, Germany.
Xuyong LinDepartment of Pathology, College of Basic Medical Sciences, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.
Xiupeng ZhangDepartment of Pathology, College of Basic Medical Sciences, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.
Xuezhu RongDepartment of Pathology, College of Basic Medical Sciences, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.
Di ZhangDepartment of Pathology, College of Basic Medical Sciences, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.
Enhua WangDepartment of Pathology, College of Basic Medical Sciences, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThough we recently reported that the WWC3 inhibits the invasiveness and metastasis of lung cancer by activating the Hippo pathway, the impact and underlying mechanisms of this process still remain unclear.

methodsTo identify the role of WWC3 in epithelial-mesenchymal transition of lung cancer, we performed immunohistochemistry to detect the expression levels of WWC3 and EMT-related biomarker, and analyzed their correlations in a cohort of 127 patients with NSCLC. Wound healing assay and cell invasion assay were applied to explore cell invasive ability change after WWC3 knockdown. qRT-PCR and immunoblotting were performed to assess mRNA and protein levels of EMT-related biomarkers and the main molecules changes of Hippo signaling caused by WWC3. Immunoprecipition was to examine WWC3 and LATS1 interaction.

resultsWWC3 knockdown drives a pronounced shift from the epithelial to the mesenchymal phenotype in lung cancer cells. In addition, WWC3 ectopic expression in lung cancer cells attenuates mesenchymal markers and increases the epithelial markers expressions; however, WWC3-ΔWW plasmid abrogated these effects. WWC3 silencing by shRNA exerts the opposite effect. Furthermore, WWC3 levels were inversely correlated with the levels of EMT inducers (Snail and Slug) in lung cancer cells and specimens. Immunoblotting revealed that WWC3 wild-type upregulates large tumor suppressor (LATS1) and yes-associated protein (YAP) phosphorylation through its WW domain, hence activating Hippo pathway. Knockdown of YAP and LATS1, as well as the as the Verteporfin (VP) usage, could reverse this effect caused by WWC3 silencing.

conclusionThese findings suggest that WWC3 works as a tumor suppressor to inhibit EMT process and confer its candidacy as a potential therapeutic target in lung cancer.

Indexed as

epithelial–mesenchymal transitionHippo pathwaynonsmall-cell lung cancerWWC3YAP

Identifiers

PMID29780251
PMCPMC5951220

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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.