Evidence map›Paper›PMID 21262926›Full record

ArticleCarcinogenesis2011

The oncogenic kinase Pim-1 is modulated by K-Ras signaling and mediates transformed growth and radioresistance in human pancreatic ductal adenocarcinoma cells.

Dapeng Xu, Stephen A Allsop, Sam M Witherspoon, Jared L Snider, Jen Jen Yeh, James J Fiordalisi, Catherine D White, Daniel Williams, Adrienne D Cox, Antonio T Baines

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Relationship between the transcriptional expression of PIM1 and local control in patients with head and neck squamous cell carcinomas treated with radiotherapy.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  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

10 authors at 4 institutions in 2 countries.

Dapeng XuDepartment of Biology, Cancer Research Program, JLC-Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.
Stephen A Allsop
Sam M Witherspoon
Jared L Snider
Jen Jen Yeh
James J Fiordalisi
Catherine D White
Daniel Williams
Adrienne D Cox
Antonio T Baines
Segeberger Kliniken · DENorth Carolina Central University · USNorth Carolina Agricultural and Technical State University · USUniversity of North Carolina at Chapel Hill · US

Funding

ROLES OF INFLAMMATION AND ANDROGEN METABOLISM IN PROSTATE CANCER DISPARITYP20MD000175 · NIMHD · NORTH CAROLINA CENTRAL UNIVERSITY · PI KIMBRO, KEVIN SEAN · 2002 to 2016
$15.6M
TISSUE PROCUREMENT &ANALYSISP50CA106991 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TEPPER, JOEL E · 2004 to 2009
$12.1M
VALIDATION OF INHIBITORS OF RHO GTPASES FOR CANCER TREATMENTU19CA067771 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI GUIDA, WAYNE · 1995 to 2009
$8.9M
MINORITY ACCESS TO RESEARCH CAREERS U*STAR PROGRAMT34GM007668 · NIGMS · NORTH CAROLINA CENTRAL UNIVERSITY · PI ROBINSON, ELWOOD L · 1985 to 2008
$2.4M
Targeting Ras-Ral GEF-Ral Effector Signaling for Pancreatic Cancer TreatmentR01CA140424 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI YEH, JEN JEN · 2010 to 2014
$1.5M
Protein prenylation, oncogenesis and novel therapeuticsR01CA109550 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COX, ADRIENNE D · 2004 to 2008
$1.2M
The Role of Pim Kinases as a Novel Molecular Target in Pancreatic CancerSC2CA137845 · NCI · NORTH CAROLINA CENTRAL UNIVERSITY · PI BAINES, ANTONIO THOMAS · 2008 to 2010
$280k
NCI NIH HHS CA106991NCI NIH HHS CA109550NCI NIH HHS CA137845NCI NIH HHS CA67771NCI NIH HHS CA92077NCI NIH HHS P50 CA106991NCI NIH HHS R01 CA109550NCI NIH HHS R01 CA140424NCI NIH HHS U19 CA067771NIGMS NIH HHS GM007668NIMHD NIH HHS MD000175
6 · The paper itself

Abstract

Oncogenic Pim-1 kinase is upregulated in multiple solid cancers, including human pancreatic ductal adenocarcinoma (PDAC), a highly lethal disease with few useful treatment options. Pim-1 is also transcriptionally induced upon oncogenic K-Ras-mediated transformation of the human pancreatic ductal epithelial (HPDE) cell model of PDAC. Given the near ubiquitous presence of mutant K-Ras in PDAC and its critical role in this disease, we wished to study the effects of oncogenic K-Ras signaling on Pim-1 expression, as well as the role of Pim-1 in growth transformation of PDAC cells. Pim-1 protein levels were upregulated in both PDAC cell lines and patient tumor tissues. Furthermore, ectopic oncogenic K-Ras increased Pim-1 expression in human pancreatic nestin-expressing (HPNE) cells, a distinct immortalized cell model of PDAC. Conversely, shRNA-mediated suppression of oncogenic K-Ras decreased Pim-1 protein in PDAC cell lines. These results indicate that oncogenic K-Ras regulates Pim-1 expression. The kinase activity of Pim-1 is constitutively active. Accordingly, shRNA-mediated suppression of Pim-1 in K-Ras-dependent PDAC cell lines decreased Pim-1 activity, as measured by decreased phosphorylation of the pro-apoptotic protein Bad and increased expression of the cyclin-dependent kinase inhibitor p27Kip1. Biological consequences of inhibiting Pim-1 expression included decreases in both anchorage-dependent and -independent cell growth, invasion through Matrigel and radioresistance as measured by standard clonogenic assays. These results indicate that Pim-1 is required for PDAC cell growth, invasion and radioresistance downstream of oncogenic K-Ras. Overall, our studies help to elucidate the role of Pim-1 in PDAC growth transformation and validate Pim-1 kinase as a potential molecular marker for mutated K-Ras activity.

Indexed as

Radiation ToleranceAdenocarcinomabcl-Associated Death ProteinCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p27HumansNeoplasm InvasivenessPancreatic NeoplasmsPhosphorylationProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1Proto-Oncogene Proteins p21(ras)ras ProteinsSignal TransductionBAD protein, humanbcl-Associated Death ProteinCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27KRAS protein, humanPIM1 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1Proto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID21262926
PMCPMC3066419
OpenAlexW2120498539

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.