PittsburghV1, Main, Exploration, bibRecord, 001911

Protein Kinase D as a Potential Chemotherapeutic Target for Colorectal Cancer

Identifieur interne : 001911 ( Main/Exploration ); précédent : 001910; suivant : 001912

Protein Kinase D as a Potential Chemotherapeutic Target for Colorectal Cancer

Auteurs : Ning Wei [États-Unis] ; Edward Chu [États-Unis] ; Peter Wipf [États-Unis] ; John C. Schmitz [États-Unis]

Source :

Molecular cancer therapeutics [ 1535-7163 ] ; 2014.

RBID : PMC:4019967

Descripteurs français

KwdFr :
- Animaux, Antinéoplasiques (pharmacologie), Apoptose (), Cycle cellulaire (), Expression des gènes, Femelle, Humains, Inhibiteurs de protéines kinases (pharmacologie), Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Prolifération cellulaire (), Protéine kinase C (antagonistes et inhibiteurs), Protéine kinase C (génétique), Protéine kinase C (métabolisme), Souris, Survie cellulaire (), Tests d'activité antitumorale sur modèle de xénogreffe, Tumeurs colorectales (génétique), Tumeurs colorectales (métabolisme), Tumeurs colorectales (traitement médicamenteux).
MESH :
- antagonistes et inhibiteurs : Protéine kinase C.
- génétique : Protéine kinase C, Tumeurs colorectales.
- métabolisme : Protéine kinase C, Tumeurs colorectales.
- pharmacologie : Antinéoplasiques, Inhibiteurs de protéines kinases.
- traitement médicamenteux : Tumeurs colorectales.
- Animaux, Apoptose, Cycle cellulaire, Expression des gènes, Femelle, Humains, Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Prolifération cellulaire, Souris, Survie cellulaire, Tests d'activité antitumorale sur modèle de xénogreffe.

English descriptors

KwdEn :
- Animals, Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Cell Cycle (drug effects), Cell Line, Tumor, Cell Proliferation (drug effects), Cell Survival (drug effects), Colorectal Neoplasms (drug therapy), Colorectal Neoplasms (genetics), Colorectal Neoplasms (metabolism), Disease Models, Animal, Female, Gene Expression, Humans, Mice, Protein Kinase C (antagonists & inhibitors), Protein Kinase C (genetics), Protein Kinase C (metabolism), Protein Kinase Inhibitors (pharmacology), Xenograft Model Antitumor Assays.
MESH :
- chemical , antagonists & inhibitors : Protein Kinase C.
- chemical , genetics : Protein Kinase C.
- chemical , metabolism : Protein Kinase C.
- chemical , pharmacology : Antineoplastic Agents, Protein Kinase Inhibitors.
- drug effects : Apoptosis, Cell Cycle, Cell Proliferation, Cell Survival.
- drug therapy : Colorectal Neoplasms.
- genetics : Colorectal Neoplasms.
- metabolism : Colorectal Neoplasms.
- Animals, Cell Line, Tumor, Disease Models, Animal, Female, Gene Expression, Humans, Mice, Xenograft Model Antitumor Assays.

Abstract

Protein kinase D (PKD) signaling plays a critical role in the regulation of DNA synthesis, proliferation, cell survival, adhesion, invasion/migration, motility, and angiogenesis. To date, relatively little is known about the potential role of PKD in the development and/or progression of human colorectal cancer (CRC). We evaluated the expression of different PKD isoforms in CRC and investigated the antitumor activity of PKD inhibitors against human CRC. PKD2 was the dominant isoform expressed in human colon cancer cells. PKD3 expression was also observed but PKD1 expression, at both the RNA and protein levels, was not detected. Suppression of PKD using the small molecule inhibitors, CRT0066101 and kb-NB142-70, resulted in low micromolar in vitro antiproliferative activity against multiple human CRC cell lines. Drug treatment was associated with dose-dependent suppression of PKD2 activation. Incubation with CRT0066101 resulted in G2/M phase arrest and induction of apoptosis in human CRC cells. Further studies showed that CRT0066101 treatment gave rise to a dose-dependent increase in expression of cleaved PARP and activated caspase-3, in addition to inhibition of AKT and ERK signaling, and suppression of NF-κB activity. Transfection of PKD2-targeted siRNAs resulted in similar effects on downstream pathways as observed with small molecule inhibitors. Daily administration of CRT0066101 resulted in significant inhibition of tumor growth in HCT116 xenograft nude mice. Taken together, our studies show that PKD plays a significant role in mediating growth signaling in CRC and may represent a novel chemotherapeutic target for the treatment of CRC.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019967

DOI: 10.1158/1535-7163.MCT-13-0880
PubMed: 24634417
PubMed Central: 4019967

Affiliations:

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<term>Expression des gènes</term>
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<term>Expression des gènes</term>
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<front><div type="abstract" xml:lang="en"><p id="P1">Protein kinase D (PKD) signaling plays a critical role in the regulation of DNA synthesis, proliferation, cell survival, adhesion, invasion/migration, motility, and angiogenesis. To date, relatively little is known about the potential role of PKD in the development and/or progression of human colorectal cancer (CRC). We evaluated the expression of different PKD isoforms in CRC and investigated the antitumor activity of PKD inhibitors against human CRC. PKD2 was the dominant isoform expressed in human colon cancer cells. PKD3 expression was also observed but PKD1 expression, at both the RNA and protein levels, was not detected. Suppression of PKD using the small molecule inhibitors, CRT0066101 and kb-NB142-70, resulted in low micromolar <italic>in vitro</italic>
 antiproliferative activity against multiple human CRC cell lines. Drug treatment was associated with dose-dependent suppression of PKD2 activation. Incubation with CRT0066101 resulted in G2/M phase arrest and induction of apoptosis in human CRC cells. Further studies showed that CRT0066101 treatment gave rise to a dose-dependent increase in expression of cleaved PARP and activated caspase-3, in addition to inhibition of AKT and ERK signaling, and suppression of NF-κB activity. Transfection of PKD2-targeted siRNAs resulted in similar effects on downstream pathways as observed with small molecule inhibitors. Daily administration of CRT0066101 resulted in significant inhibition of tumor growth in HCT116 xenograft nude mice. Taken together, our studies show that PKD plays a significant role in mediating growth signaling in CRC and may represent a novel chemotherapeutic target for the treatment of CRC.</p>
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Protein Kinase D as a Potential Chemotherapeutic Target for Colorectal Cancer

Protein Kinase D as a Potential Chemotherapeutic Target for Colorectal Cancer

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Abstract

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