Evidence map›Paper›PMID 25109354›Full record

ArticleOncology reports2014

CIP2A regulates cell proliferation via the AKT signaling pathway in human lung cancer.

Ningjing Lei, Bo Peng, Jian-Ying Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  5. Review
  6. Review
  7. Article
  8. Article
  9. PP2Ac upregulates PI3K-Akt signaling and induces hepatocyte apoptosis in liver donor after brain death.Apoptosis : an international journal on programmed cell death · 2019
    Article
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  18. Pluripotency transcription factors in lung cancer-a review.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Ningjing LeiBorder Biomedical Research Center and Department of Biological Sciences, The University of Texas at El Paso, El Paso, TX 79968, USA.
Bo PengBorder Biomedical Research Center and Department of Biological Sciences, The University of Texas at El Paso, El Paso, TX 79968, USA.
Jian-Ying ZhangBorder Biomedical Research Center and Department of Biological Sciences, The University of Texas at El Paso, El Paso, TX 79968, USA.
The University of Texas at El Paso · US

Funding

TCCG12MD007592 · NIMHD · UNIVERSITY OF TEXAS EL PASO · PI KIRKEN, ROBERT A. · 2012 to 2018
$19.4M
Autoantibodies to tumor-associated antigens as diagnostic biomarkers in liver canSC1CA166016 · NCI · UNIVERSITY OF TEXAS EL PASO · PI ZHANG, JIANYING · 2011 to 2014
$1.0M
NCI NIH HHS SC1 CA166016NIMHD NIH HHS 5G12MD007592NIMHD NIH HHS G12 MD007592
6 · The paper itself

Abstract

Cancerous inhibitor of PP2A (CIP2A) is an intracellular endogenous protein phosphatase 2A (PP2A) inhibitor with oncogenic activities. Initially identified as a tumor-associated antigen (TAA) in gastric and liver cancer patients, CIP2A was overexpressed in a variety of cancer types. The overexpression of CIP2A in cancer cells is associated with increased cell proliferation. However, the mechanism of CIP2A in cancer cell proliferation remains poorly understood. In the present study, we reported that CIP2A can regulate AKT phosphorylation at S473 under growth factor stimulation and our results also showed that CIP2A may promote cell proliferation through the AKT signaling pathway. Notably, depletion of CIP2A did not induce a global change of AKT phosphatase activity, which indicated that CIP2A may recognize specific AKT targets and play certain roles in the signaling pathway. In addition, we detected that CIP2A expression was associated with mTOR phosphorylation. Our further analysis corroborated the relationship between CIP2A and AKT-mTOR signaling pathway. Therefore, our study addressed a novel role of CIP2A in mediating cancer progression through interacting with the AKT-mTOR signaling pathway.

Indexed as

AutoantigensCell Line, TumorCell ProliferationGene Knockdown TechniquesHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMembrane ProteinsProto-Oncogene Proteins c-aktRNA, Small InterferingSignal TransductionTOR Serine-Threonine KinasesAutoantigensCIP2A protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsMTOR protein, humanProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID25109354
PMCPMC4148383
OpenAlexW2077968895

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.