Evidence map›Paper›PMID 27041574›Full record

ArticleOncogene2016

PRR14 is a novel activator of the PI3K pathway promoting lung carcinogenesis.

M Yang, M Lewinska, X Fan, J Zhu, Z-M Yuan

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.2field-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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
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

5 authors at 1 institution in 1 country.

M YangDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
M LewinskaDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
X FanDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
J ZhuDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Z-M YuanDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Harvard University · US

Funding

MOLECULAR BASIS OF P53 INDUCTION TO DNA DAMAGER01CA085679 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI YUAN, ZHI-MIN · 2001 to 2015
$3.4M
A p53/NFkB-mediated metabolic mechanism for chemotherapy protectionR01CA183074 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI YUAN, ZHI-MIN · 2014 to 2018
$1.7M
Modulation of p53 function by tyrosine kinase networksR01CA167814 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI YUAN, ZHI-MIN · 2012 to 2016
$1.6M
The role of beclin 1/class III PI-3 kinase and p53 in breast tumorigenesisR01CA125144 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI YUAN, ZHI-MIN · 2008 to 2012
$1.5M
NCI NIH HHS R01 CA085679NCI NIH HHS R01 CA125144NCI NIH HHS R01 CA167814NCI NIH HHS R01 CA183074
6 · The paper itself

Abstract

Chromosomal focal amplifications often cause an increase in gene copy number, contributing to the pathogenesis of cancer. PRR14 overexpression is associated with recurrent locus amplification in lung cancer, and it correlates with a poor prognosis. We show that increased PRR14 expression promoted and reduced PRR14 expression impeded lung cancer cell proliferation. Interestingly, PRR14 cells were markedly enlarged in size and exhibited an elevated activity of the PI3-kinase/Akt/mTOR pathway, which was associated with a heightened sensitivity to the inhibitors of PI3K and mammalian target of rapamycin (mTOR). Biochemical analysis revealed that PRR14, as a proline-rich protein, binds to the Src homology 3 (SH3) domains of GRB2 resulting in PI3K activation. Significantly, two cancer patient-derived PRR14 mutants displayed considerably augmented GRB2-binding and an enhanced ability of promoting cell proliferation. Together with the in vivo data demonstrating a strong tumor-promoting activity of PRR14 and the mutants, our work uncovered this proline-rich protein as a novel activator of the PI3K pathway that promoted tumorigenesis in lung cancer.

Indexed as

Cell Transformation, NeoplasticSignal TransductionAnimalsCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneCluster AnalysisDisease Models, AnimalGene AmplificationGene ExpressionGene Expression ProfilingGRB2 Adaptor ProteinHeterograftsHumansLung NeoplasmsMiceChromosomal Proteins, Non-HistoneGRB2 Adaptor ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPRR14 protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID27041574
PMCPMC5787860
OpenAlexW2337140503

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.