Evidence map›Paper›PMID 24777602›Full record

ArticleMolecular and cellular biology2014

The Pim-1 protein kinase is an important regulator of MET receptor tyrosine kinase levels and signaling.

Bo Cen, Ying Xiong, Jin H Song, Sandeep Mahajan, Rachel DuPont, Kristen McEachern, Daniel J DeAngelo, Jorge E Cortes, Mark D Minden, Allen Ebens and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  9. Interleukin (IL)-7 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Article
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  14. The role of Pim kinase in immunomodulation.American journal of cancer research · 2020
    Review
  15. Article
  16. Phosphorylation of DEPDC5, a component of the GATOR1 complex, releases inhibition of mTORC1 and promotes tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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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

13 authors at 6 institutions in 2 countries.

Bo CenDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA The Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina, USA cen@musc.edu kraft@musc.edu.
Ying XiongDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Jin H SongDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, USA The Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina, USA.
Sandeep MahajanThe Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina, USA.
Rachel DuPontOncology iMed, AstraZeneca, Waltham, Massachusetts, USA.
Kristen McEachernOncology iMed, AstraZeneca, Waltham, Massachusetts, USA.
Daniel J DeAngeloDana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.
Jorge E CortesDepartment of Leukemia, University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.
Mark D MindenPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Allen EbensGenentech, Inc., South San Francisco, California, USA.
Alice MimsDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Amanda C LaRueThe Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina, USA Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina, USA Research Services, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, USA.
Andrew S KraftDepartment of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA The Hollings Cancer Center, Medical University of South Carolina, Charleston, South Carolina, USA cen@musc.edu kraft@musc.edu.
Medical University of South Carolina · USAstraZeneca (United States) · USMUSC Hollings Cancer Center · USDana-Farber Cancer Institute · USPrincess Margaret Cancer Centre · CAThe University of Texas MD Anderson Cancer Center · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Jian Ouyang · 2009 to 2026
$42.7M
Targeting the Pim 1 Protein Kinase to Overcome Resistance to AKT InhibitorsR01CA173200 · NCI · UNIVERSITY OF ARIZONA · PI KRAFT, ANDREW S · 2013 to 2017
$1.6M
Hematopoietic Stem Cell-Derived Carcinoma Associated Fibroblasts in TumorR01CA148772 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LARUE, AMANDA C. · 2011 to 2015
$1.3M
Role of Pim Kinases in Prostate Epithelium GrowthK01DK085196 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CEN, BO · 2011 to 2014
$531k
NCI NIH HHS 1R01CA173200NCI NIH HHS 5P30CA138313NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA148772NCI NIH HHS R01 CA173200NIDDK NIH HHS 1K01DK085196NIDDK NIH HHS K01 DK085196
6 · The paper itself

Abstract

MET, the receptor for hepatocyte growth factor (HGF), plays an important role in signaling normal and tumor cell migration and invasion. Here, we describe a previously unrecognized mechanism that promotes MET expression in multiple tumor cell types. The levels of the Pim-1 protein kinase show a positive correlation with the levels of MET protein in human tumor cell lines and patient-derived tumor materials. Using small interfering RNA (siRNA), Pim knockout mice, small-molecule inhibitors, and overexpression of Pim-1, we confirmed this correlation and found that Pim-1 kinase activity regulates HGF-induced tumor cell migration, invasion, and cell scattering. The novel biochemical mechanism for these effects involves the ability of Pim-1 to control the translation of MET by regulating the phosphorylation of eukaryotic initiation factor 4B (eIF4B) on S406. This targeted phosphorylation is required for the binding of eIF4B to the eIF3 translation initiation complex. Importantly, Pim-1 action was validated by the evaluation of patient blood and bone marrow from a phase I clinical trial of a Pim kinase inhibitor, AZD1208. These results suggest that Pim inhibitors may have an important role in the treatment of patients where MET is driving tumor biology.

Indexed as

AnimalsBiphenyl CompoundsCell Line, TumorCell MovementEukaryotic Initiation Factor-3Eukaryotic Initiation FactorsHeLa CellsHepatocyte Growth FactorHumansMiceMice, KnockoutNeoplasm InvasivenessPhosphorylationProtein BindingProtein BiosynthesisProtein Kinase InhibitorsAZD1208Biphenyl CompoundseIF-4BEukaryotic Initiation Factor-3Eukaryotic Initiation FactorsHepatocyte Growth FactorPim1 protein, mouseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metProto-Oncogene Proteins c-pim-1RNA, Small InterferingThiazolidines

Identifiers

PMID24777602
PMCPMC4054323
OpenAlexW2100170827

What OpenQuestion holds

Textmetadata
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.