Evidence map›Paper›PMID 20103639›Full record

ArticleCancer research2010

Silencing of RON receptor signaling promotes apoptosis and gemcitabine sensitivity in pancreatic cancers.

Jocelyn Logan-Collins, Ryan M Thomas, Peter Yu, Dawn Jaquish, Evangeline Mose, Randall French, William Stuart, Rebecca McClaine, Bruce Aronow, Robert M Hoffman and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  6. The HNRNPA2B1-MST1R-Akt axis contributes to epithelial-to-mesenchymal transition in head and neck cancer.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
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  10. Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2019
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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

12 authors at 4 institutions in 1 country.

Jocelyn Logan-CollinsDepartment of Surgery, Division of Surgical Oncology, University of Cincinnati, Ohio, USA.
Ryan M Thomas
Peter Yu
Dawn Jaquish
Evangeline Mose
Randall French
William Stuart
Rebecca McClaine
Bruce Aronow
Robert M Hoffman
Susan E Waltz
Andrew M Lowy
University of California, San Diego · USUniversity of Cincinnati Medical Center · USAntiCancer (United States) · USCincinnati Children's Hospital Medical Center · US

Funding

REGULATION OF TUMOR CELL ATTACHMENT BY SURFACE ANTIGENSR01CA045726 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHERESH, DAVID A · 1988 to 2017
$7.4M
The Ron Receptor in Mammary Gland BiologyR01CA100002 · NCI · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2004 to 2008
$1.5M
Research in Alimentary Tract SurgeryT32DK064581 · NIDDK · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2003 to 2007
$1.1M
Gene Targets of Wnt Signaling in Pancreatic CancerK08CA089403 · NCI · UNIVERSITY OF CINCINNATI · PI LOWY, ANDREW M · 2001 to 2006
$689k
Targeting RON Receptor Signaling in Pancreatic CancerR21CA137692 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOWY, ANDREW M · 2009 to 2010
$340k
NCI NIH HHS CA100002NCI NIH HHS CA 45726NCI NIH HHS CA89403NCI NIH HHS K08 CA089403NCI NIH HHS R01 CA045726NCI NIH HHS R01 CA100002NCI NIH HHS R21 CA137692NIDDK NIH HHS T32 DK064581NIDDK NIH HHS T32 DK64581
6 · The paper itself

Abstract

The RON receptor tyrosine kinase is overexpressed in premalignant pancreatic intraepithelial neoplasia (PanIN) and in the majority of pancreatic cancers. In pancreatic cells, RON is an important K-Ras effector and RON ligand can enhance migration/invasion and apoptotic resistance. However, the pathobiological significance of RON overexpression in pancreatic cancers has yet to be fully established. In this study, we demonstrate that RON signaling mediates a unique transcriptional program that is conserved between cultured cells derived from murine PanIN or human pancreatic cancer cells grown as subcutaneous tumor xenografts. In both systems, RON signaling regulates expression of genes implicated in cancer-cell survival, including Bcl-2 and the transcription factors signal transducer and activator of transcription 3 (STAT 3) and c-Jun. shRNA-mediated silencing of RON in pancreatic cancer xenografts inhibited their growth, primarily by increasing susceptibility to apoptosis and by sensitizing them to gemcitabine treatment. Escape from RON silencing was associated with re-expression of RON and/or expression of phosphorylated forms of the related c-Met or epidermal growth factor receptors. These findings indicate that RON signaling mediates cell survival and in vivo resistance to gemcitabine in pancreatic cancer, and they reveal mechanisms through which pancreatic cancer cells may circumvent RON-directed therapies.

Indexed as

Signal TransductionAnimalsAntimetabolites, AntineoplasticApoptosisCell Line, TumorCell ProliferationCluster AnalysisDeoxycytidineGemcitabineGene Expression ProfilingHumansImmunoblottingMiceMice, NudeOligonucleotide Array Sequence AnalysisPancreatic NeoplasmsAntimetabolites, AntineoplasticDeoxycytidineGemcitabineReceptor Protein-Tyrosine KinasesRON protein

Identifiers

PMID20103639
PMCPMC2943733
OpenAlexW2097644281

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.