Evidence map›Paper›PMID 26983689›Full record

ArticleMolecular cancer research : MCR2016

Kinase-Dependent and -Independent Roles for PTK6 in Colon Cancer.

Priya S Mathur, Jessica J Gierut, Grace Guzman, Hui Xie, Rosa M Xicola, Xavier Llor, Michael I Chastkofsky, Ansu O Perekatt, Angela L Tyner

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

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  15. Review
  16. Targeting protein tyrosine kinase 6 in cancer.Biochimica et biophysica acta. Reviews on cancer · 2020
    Review
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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 2 institutions in 1 country.

Priya S MathurDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois.
Jessica J GierutDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois.
Grace GuzmanDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois.
Hui XieDepartment of Epidemiology and Biostatistics, University of Illinois at Chicago, Chicago, Illinois.
Rosa M XicolaDepartment of Internal Medicine, Yale University, New Haven, Connecticut.
Xavier LlorDepartment of Internal Medicine, Yale University, New Haven, Connecticut.
Michael I ChastkofskyDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois.
Ansu O PerekattDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois.
Angela L TynerDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois. atyner@uic.edu.
University of Illinois Chicago · USYale University · US

Funding

ISOLATION OF GENETIC MARKERS FOR INTESTINAL CRYPT CELLSR01DK044525 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI TYNER, ANGELA L · 1993 to 2016
$4.8M
NIDDK NIH HHS R01 DK044525
6 · The paper itself

Abstract

unlabelledDisruption of the gene encoding Protein Tyrosine Kinase 6 (Ptk6) delayed differentiation and increased growth in the mouse intestine. However, Ptk6-null mice were also resistant to azoxymethane-induced colon tumorigenesis. To further explore functions of PTK6 in colon cancer, expression of epithelial and mesenchymal markers, as well as proliferation, migration, and xenograft tumor growth, was examined in human colon tumor cell lines with knockdown or overexpression of PTK6. PTK6 protein, transcript, and activation were also examined in a human colon tumor tissue array, using immunohistochemistry and qRT-PCR. Knockdown of PTK6 led to the epithelial-mesenchymal transition (EMT) in SW480 and HCT116 cells, whereas overexpression of PTK6 in SW620 cells restored an epithelial phenotype in a kinase-independent manner. PTK6 knockdown also increased xenograft tumor growth of SW480 cells, suggesting tumor suppressor functions. In clinical specimens, PTK6 expression was highest in normal differentiated epithelial cells and reduced in tumors. In contrast, overexpression of constitutively active PTK6 promoted STAT3 and ERK5 activation in colon cancer cells, and endogenous PTK6 promoted cell survival and oncogenic signaling in response to DNA-damaging treatments. These data indicate that PTK6 has complex, context-specific functions in colon cancer; PTK6 promotes the epithelial phenotype to antagonize the EMT in a kinase-independent manner, whereas activation of PTK6 promotes oncogenic signaling. IMPLICATIONS: Understanding context-specific functions of PTK6 is important, because although it promotes cell survival and oncogenic signaling after DNA damage, expression of PTK6 in established tumors may maintain the epithelial phenotype, preventing tumor progression. Mol Cancer Res; 14(6); 563-73. ©2016 AACR.

Indexed as

AnimalsCell Line, TumorColonic NeoplasmsFemaleHCT116 CellsHeterograftsHumansMiceMice, NudeNeoplasm ProteinsProtein-Tyrosine KinasesSignal TransductionNeoplasm ProteinsProtein-Tyrosine KinasesPTK6 protein, human

Identifiers

PMID26983689
PMCPMC4912439
OpenAlexW2302318537

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Registered trials

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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.