Evidence map›Paper›PMID 28875501›Full record

ArticleThe Prostate2017

The protein kinase C super-family member PKN is regulated by mTOR and influences differentiation during prostate cancer progression.

Chun-Song Yang, Tiffany A Melhuish, Adam Spencer, Li Ni, Yi Hao, Kasey Jividen, Thurl E Harris, Chelsi Snow, Henry F Frierson, David Wotton and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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  15. Biomolecular NMR assignments · 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

11 authors at 1 institution in 1 country.

Chun-Song YangCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Tiffany A MelhuishCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Adam SpencerCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Li NiCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Yi HaoCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Kasey JividenCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Thurl E HarrisDepartment of Pharmacology, University of Virginia, Charlottesville, Virginia.
Chelsi SnowCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Henry F FriersonDepartment of Pathology, University of Virginia, Charlottesville, Virginia.
David WottonCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
Bryce M PaschalCenter for Cell Signaling, University of Virginia, Charlottesville, Virginia.
University of Virginia · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
VEGF, FAK and RAPP01CA104106 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI PASCHAL, BRYCE, THEODORESCU, DAN · 2005 to 2015
$17.9M
Cancer Research Training Program: From Molecular Mechanisms to Therapeutic StrategiesT32CA009109 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Andrew Carl Dudley, Melanie R Rutkowski · 1985 to 2026
$13.9M
TRAINING IN CELL AND MOLECULAR BIOLOGYT32GM008136 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI STUKENBERG, P. TODD · 1985 to 2020
$8.5M
Role of Oxidized neutral lipids in adipocyte functionR01DK101946 · NIDDK · UNIVERSITY OF VIRGINIA · PI HARRIS, THURL E. · 2014 to 2018
$1.7M
Regulation of neural development by TGF beta family signalingR01NS077958 · NINDS · UNIVERSITY OF VIRGINIA · PI WOTTON, DAVID · 2012 to 2016
$1.7M
NCI NIH HHS P01 CA104106NCI NIH HHS P30 CA044579NCI NIH HHS T32 CA009109NIDDK NIH HHS R01 DK101946NIGMS NIH HHS T32 GM008136NINDS NIH HHS R01 NS077958
6 · The paper itself

Abstract

backgroundPhosphoinositide-3 (PI-3) kinase signaling has a pervasive role in cancer. One of the key effectors of PI-3 kinase signaling is AKT, a kinase that promotes growth and survival in a variety of cancers. Genetically engineered mouse models of prostate cancer have shown that AKT signaling is sufficient to induce prostatic epithelial neoplasia (PIN), but insufficient for progression to adenocarcinoma. This contrasts with the phenotype of mice with prostate-specific deletion of Pten, where excessive PI-3 kinase signaling induces both PIN and locally invasive carcinoma. We reasoned that additional PI-3 kinase effector kinases promote prostate cancer progression via activities that provide biological complementarity to AKT. We focused on the PKN kinase family members, which undergo activation in response to PI-3 kinase signaling, show expression changes in prostate cancer, and contribute to cell motility pathways in cancer cells.

methodsPKN kinase activity was measured by incorporation of RESULTS AND

conclusionsPKN1 and PKN2 contribute to motility pathways in human prostate cancer cells. PKN1 and PKN2 kinase activity is regulated by TORC2-dependent phosphorylation of the TM, which together with published data indicates that PKN proteins receive multiple PI-3 kinase-dependent inputs. Transgenic expression of active AKT and PKN1 is not sufficient for progression beyond PIN. Moreover, Pkn1 is not required for tumorigenesis initiated by loss of Pten. Triple knockout of Pten, Pkn1, and Pkn2 in mouse prostate results in squamous cell carcinoma, an uncommon but therapy-resistant form of prostate cancer.

Indexed as

AnimalsCell DifferentiationDisease ProgressionHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, TransgenicProstatic NeoplasmsProtein Kinase CPTEN PhosphohydrolaseTOR Serine-Threonine KinasesMTOR protein, humanProtein Kinase Cprotein kinase NPTEN PhosphohydrolasePTEN protein, humanPten protein, mouseTOR Serine-Threonine Kinasesmouse modelsphosphorylationPI-3 kinasesquamous cell carcinoma

Identifiers

PMID28875501
PMCPMC5669364
OpenAlexW2753004361

What OpenQuestion holds

Textmetadata
LicenceTDM
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.