Evidence map›Paper›PMID 26859575›Full record

ArticleOncotarget2016

The sonic hedgehog signaling pathway stimulates anaplastic thyroid cancer cell motility and invasiveness by activating Akt and c-Met.

Ashley J Williamson, Michelle E Doscas, Jin Ye, Katherine B Heiden, Mingzhao Xing, Yi Li, Richard A Prinz, Xiulong Xu

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 37 citations in OpenAlex.

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  13. The Role of Hedgehog Pathway in Female Cancers.Journal of cancer science and clinical therapeutics · 2020
    Article
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  15. Article
  16. Crosstalk between Hh and Wnt signaling promotes osteosarcoma progression.International journal of clinical and experimental pathology · 2019
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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

8 authors at 5 institutions in 2 countries.

Ashley J WilliamsonRush Medical College, Rush University Medical Center, Chicago, IL, USA.
Michelle E DoscasDepartment of Anatomy and Cell Biology, Rush University Medical Center, Chicago, IL, USA.
Jin YeDepartment of Anatomy and Cell Biology, Rush University Medical Center, Chicago, IL, USA.
Katherine B HeidenDepartment of General Surgery, Rush University Medical Center, Chicago, IL, USA.
Mingzhao XingDivision of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Yi LiLester and Sue Smith Breast Center and Department of Molecular and Cell Biology, Baylor College of Medicine, Houston, TX, USA.
Richard A PrinzDepartment of Surgery, NorthShore University Health System, Evanston, IL, USA.
Xiulong XuCenter for Comparative Medicine, College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu Province, China.
Rush University Medical Center · USBaylor College of Medicine · USJohns Hopkins Medicine · USNorthShore University HealthSystem · USYangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sonic hedgehog (Shh) pathway is highly activated in thyroid neoplasms and promotes thyroid cancer stem-like cell phenotype, but whether the Shh pathway regulates thyroid tumor cell motility and invasiveness remains unknown. Here, we report that the motility and invasiveness of two anaplastic thyroid tumor cell lines, KAT-18 and SW1736, were inhibited by two inhibitors of the Shh pathway (cyclopamine and GANT61). Consistently, the cell motility and invasiveness was decreased by Shh and Gli1 knockdown, and was increased by Gli1 overexpression in KAT-18 cells. Mechanistic studies revealed that Akt and c-Met phosphorylation was decreased by a Gli1 inhibitor and by Shh and Gli1 knockdown, but was increased by Gli1 overexpression. LY294002, a PI-3 kinase inhibitor, and a c-Met inhibitor inhibited the motility and invasiveness of Gli1-transfected KAT-18 cells more effectively than the vector-transfected cells. Knockdown of Snail, a transcription factor regulated by the Shh pathway, led to decreased cell motility and invasiveness in KAT-18 and SW1736 cells. However, key epithelial-to-mesenchymal transition (EMT) markers including E-cadherin and vimentin as well as Slug were not affected by cyclopamine and GANT61 in either SW1736 or WRO82, a well differentiated follicular thyroid carcinoma cell line. Our data suggest that the Shh pathway-stimulated thyroid tumor cell motility and invasiveness is largely mediated by AKT and c-Met activation with little involvement of EMT.

Indexed as

CadherinsCell Line, TumorCell MovementChromonesEnzyme ActivationEpithelial-Mesenchymal TransitionHedgehog ProteinsHumansMorpholinesNeoplasm InvasivenessPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metPyridinesPyrimidinesSignal Transduction2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCadherinsChromonescyclopamineGANT 61GLI1 protein, humanHedgehog ProteinsMET protein, humanMorpholinesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metPyridinesPyrimidinesSHH protein, humanSNAI1 protein, humanSnail Family Transcription FactorsVeratrum AlkaloidsVimentinZinc Finger Protein GLI1cell motility and invasionc-MetPI-3 kinaseSnailsonic hedgehog signaling pathway

Identifiers

PMID26859575
PMCPMC4891133
OpenAlexW2290576868

What OpenQuestion holds

Textmetadata
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.