Evidence map›Paper›PMID 28288645›Full record

ArticleMolecular cancer2017

Mesothelin promotes epithelial-to-mesenchymal transition and tumorigenicity of human lung cancer and mesothelioma cells.

Xiaoqing He, Liying Wang, Heimo Riedel, Kai Wang, Yong Yang, Cerasela Zoica Dinu, Yon Rojanasakul

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 130 citations in OpenAlex.

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  20. Mesothelin promotes brain metastasis of non-small cell lung cancer by activating MET.Journal of experimental & clinical cancer research : CR · 2024
    Article

8 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Xiaoqing HeDepartment of Pharmaceutical Sciences, West Virginia University, 1 Medical Center Drive, Morgantown, WV, 26506, USA.
Liying WangHELD, National Institute for Occupational Safety and Health, CDC, 1095 Willowdale Road, Morgantown, WV, 26505, USA.
Heimo RiedelDepartment of Biochemistry, West Virginia University, Morgantown, USA.
Kai WangDepartment of Chemical and Biochemical Engineering, West Virginia University, 395 Evansdale Drive, Morgantown, WV, 26506, USA.
Yong YangDepartment of Chemical and Biochemical Engineering, West Virginia University, 395 Evansdale Drive, Morgantown, WV, 26506, USA.
Cerasela Zoica DinuDepartment of Chemical and Biochemical Engineering, West Virginia University, 395 Evansdale Drive, Morgantown, WV, 26506, USA.
Yon RojanasakulDepartment of Pharmaceutical Sciences, West Virginia University, 1 Medical Center Drive, Morgantown, WV, 26506, USA. yrojan@hsc.wvu.edu.
West Virginia University · USNational Institute for Occupational Safety and Health · USWest Virginia University Hospitals · US

Funding

WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
THE ROLE OF HEF1 PROTEIN IN INVASION OF METASTATIC BREAST CANCERP20RR016440 · NCRR · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2001 to 2010
$22.8M
West Virginia Flow Cytometry Core FacilityP30GM103488 · NIGMS · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2012 to 2016
$4.8M
Induction of Neoplastic Transformation and Cancer Stem Cells by Carbon NanotubesR01ES022968 · NIEHS · WEST VIRGINIA UNIVERSITY · PI ROJANASAKUL, YON · 2014 to 2019
$1.7M
Nanoparticle Fibrogenicity and Fibroblast Stem-Like CellsR01EB018857 · NIBIB · WEST VIRGINIA UNIVERSITY · PI ROJANASAKUL, YON · 2016 to 2019
$1.3M
COBRE FOR SIGNAL TRANSDUCTION AND CANCER PHASE IIIP30RR032138 · NCRR · WEST VIRGINIA UNIVERSITY · PI GIBSON, LAURA F. · 2011 to 2011
$1.1M
Biomimetic Alveolar Interstitium Model for Investigation of Nanomaterials-induced FibrogenesisR15GM122953 · NIGMS · WEST VIRGINIA UNIVERSITY · PI YANG, YONG · 2016 to 2016
$431k
NCRR NIH HHS P20 RR016440NCRR NIH HHS P20 RR016477NCRR NIH HHS P30 RR032138NIBIB NIH HHS R01 EB018857NIEHS NIH HHS R01 ES022968NIGMS NIH HHS P30 GM103488NIGMS NIH HHS R15 GM122953
6 · The paper itself

Abstract

backgroundLung cancer and pleural mesothelioma are two of the most deadly forms of cancer. The prognosis of lung cancer and mesothelioma is extremely poor due to limited treatment modalities and lack of understanding of the disease mechanisms. We have identified mesothelin as a potentially unique therapeutic target that as a specific advantage appears nonessential in most cell types. Mesothelin (MSLN), a plasma membrane differentiation antigen, is expressed at a high level in many human solid tumors, including 70% of lung cancer and nearly all mesotheliomas. However, the role of MSLN in the disease process and underlying mechanisms is largely unknown.

methodsShRNA knockdown and overexpression of MSLN were performed in human cancer cell lines and corresponding normal cells, respectively. Tumorigenic and metastatic effects of MSLN were examined by tumor sphere formation, migration, and invasion assays in vitro, as well as xenograft tumor assay in vivo. EMT and CSCs were detected by qPCR array, immunoblotting and flow cytometry.

resultsMSLN plays a key role in controlling epithelial-to-mesenchymal transition (EMT) and stem properties of human lung cancer and mesothelioma cells that control their tumorigenicity and metastatic potential. Firstly, MSLN was found to be highly upregulated in non-small cell lung cancer (NSCLC) patient tissues and in lung carcinoma and mesothelioma cell lines. Secondly, genetic knockdown of MSLN significantly reduced anchorage-independent cell growth, tumor sphere formation, cell adhesion, migration and invasion in vitro, as well as tumor formation and metastasis in vivo. Thirdly, ectopic overexpression of MSLN induced the malignant phenotype of non-cancerous cells, supporting its role as an oncogene. Finally, mechanistic studies revealed that knockdown of MSLN reversed EMT and attenuated stem cell properties, in addition to inhibiting tumor growth and metastasis.

conclusionsThese results indicate an essential role of MSLN in controlling EMT and stem cell properties of human lung cancer and mesothelioma cells. Since EMT is an important process in tumor progression and metastasis, and MSLN is nonessential in most normal tissue, our findings on MSLN may provide new insights into the disease mechanisms and may aid in the development of novel targeted therapy for lung cancer and mesothelioma.

Indexed as

AnimalsCell AdhesionCell Line, TumorCell MovementCell Transformation, NeoplasticDisease Models, AnimalEpithelial-Mesenchymal TransitionGene ExpressionGene Knockdown TechniquesGPI-Linked ProteinsHeterograftsHumansLung NeoplasmsMesothelinMesotheliomaMiceGPI-Linked ProteinsMesothelinMSLN protein, humanMsln protein, mouseCancer stem cellsCirculating tumor cellsEpithelial to mesenchymal transitionLung cancerMesothelinMesotheliomaMetastasis

Identifiers

PMID28288645
PMCPMC5348784
OpenAlexW2595525832

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.