Evidence map›Paper›PMID 20082306›Full record

ArticleJournal of cellular physiology2010

Induced overexpression of protein kinase D1 stimulates mitogenic signaling in human pancreatic carcinoma PANC-1 cells.

Krisztina Kisfalvi, Cliff Hurd, Sushovan Guha, Enrique Rozengurt

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024
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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

4 authors at 2 institutions in 1 country.

Krisztina KisfalviDivision of Digestive Diseases, Department of Medicine, CURE: Digestive Diseases Research Center, David Geffen School of Medicine, Molecular Biology Institute, University of California, Los Angeles, California 90095-1786, USA.
Cliff Hurd
Sushovan Guha
Enrique Rozengurt
University of California, Los Angeles · USThe University of Texas MD Anderson Cancer Center · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
GASTROINTESTINAL PEPTIDE SIGNALING THROUGH PKC/PKDR01DK055003 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1999 to 2011
$4.9M
GI PEPTIDE SIGNALING THROUGH TYROSINE PHOSPHORYLATIONR01DK056930 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 2000 to 2010
$3.0M
Targeting crosstalk between insulin and Gq signaling systems in pancreatic cancerR21CA137292 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 2009 to 2010
$373k
NCI NIH HHS R21 CA137292NCI NIH HHS R21CA137292NIDDK NIH HHS P30 DK041301NIDDK NIH HHS P30DK41301NIDDK NIH HHS R01 DK055003NIDDK NIH HHS R01 DK056930NIDDK NIH HHS R01DK55003NIDDK NIH HHS R01DK56930
6 · The paper itself

Abstract

Neurotensin (NT) stimulates protein kinase D1 (PKD1), extracellular signal regulated kinase (ERK), c-Jun N-terminal Kinase (JNK), and DNA synthesis in the human pancreatic adenocarcinoma cell line PANC-1. To determine the effect of PKD1 overexpression on these biological responses, we generated inducible stable PANC-1 clones that express wild-type (WT) or kinase-dead (K618N) forms of PKD1 in response to the ecdysone analog ponasterone-A (PonA). NT potently stimulated c-Jun Ser(63) phosphorylation in both wild type and clonal derivatives of PANC-1 cells. PonA-induced expression of WT, but not K618N PKD1, rapidly blocked NT-mediated c-Jun Ser(63) phosphorylation either at the level of or upstream of MKK4, a dual-specificity kinase that leads to JNK activation. This is the first demonstration that PKD1 suppresses NT-induced JNK/cJun activation in PANC-1 cells. In contrast, PKD1 overexpression markedly increased the duration of NT-induced ERK activation in these cells. The reciprocal influence of PKD1 signaling on pro-mitogenicERK and pro-apopotic JNK/c-Jun pathways prompted us to examine whether PKD1 overexpression promotes DNA synthesis and proliferation of PANC-1 cells. Our results show that PKD1 overexpression increased DNA synthesis and cell numbers of PANC-1 cells cultured in regular dishes or in polyhydroxyethylmethacrylate [Poly-(HEMA)]-coated dishes to eliminate cell adhesion (anchorage-independent growth). Furthermore, PKD1 overexpression markedly enhanced DNA synthesis induced by NT (1-10 nM). These results indicate that PKD1 mediates mitogenic signaling in PANC-1 and suggests that this enzyme could be a novel target for the development of therapeutic drugs that restrict the proliferation of these cells.

Indexed as

CarcinomaCell CountCell Line, TumorCell ProliferationCell Transformation, NeoplasticDNADNA ReplicationEcdysteroneExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGrowth SubstancesHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4NeurotensinDNAEcdysteroneExtracellular Signal-Regulated MAP KinasesGrowth SubstancesJNK Mitogen-Activated Protein KinasesMAP2K4 protein, humanMAP Kinase Kinase 4Neurotensinponasterone AProtein Kinase Cprotein kinase D

Identifiers

PMID20082306
PMCPMC2888293
OpenAlexW2080558800

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.