Protein kinase C alpha (PKCα) regulates growth and invasion of endometrial cancer cells

2009 ◽  
Vol 220 (1) ◽  
pp. 112-118 ◽  
Author(s):  
James M. Haughian ◽  
Andrew P. Bradford
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Kinase C ◽  
Protein Kinase C Alpha

scholarly journals Protein kinase C-independent stimulation of activator protein-1 and c-Jun N-terminal kinase activity in human endometrial cancer cells by the LHRH agonist triptorelin

2001 ◽  
pp. 651-658 ◽  
Author(s):  
C Grundker ◽  
L Schlotawa ◽  
V Viereck ◽  
G Emons
Keyword(s):  
Cell Proliferation ◽  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Fold Increase ◽  
Lhrh Agonist ◽  
Activator Protein 1 ◽  
Kinase C ◽  
Lhrh Receptor

OBJECTIVE: The expression of luteinizing hormone-releasing hormone (LHRH) and its receptor as a part of an autocrine regulatory system of cell proliferation has been demonstrated in a number of human malignant tumours, including cancers of the endometrium. The signalling pathway through which LHRH acts in endometrial cancer is distinct from that in pituitary gonadotrophs. The LHRH receptor interacts with the mitogenic signal transduction of growth factor receptors via activation of a phosphotyrosine phosphatase, resulting in down-regulation of cancer cell proliferation. In addition, LHRH activates nucleus factor kappaB (NFkappaB) and protects the cancer cells from apoptosis. This study was conducted to investigate additional signalling mechanisms of the LHRH receptor cooperating with NFkappaB in endometrial cancer cells. DESIGN: The LHRH agonist triptorelin-induced activator protein-1 (AP-1) activation was analysed using a pAP-1-SEAP reporter gene assay. Expression of c-jun mRNA was quantified using quantitative reverse transcription (RT)-PCR. c-Jun N-terminal kinase (JNK) activity was measured by quantification of phosphorylated c-Jun protein. RESULTS: Treatment of Ishikawa and Hec-1A human endometrial cancer cells with 100 nM triptorelin resulted in a 3.1-fold and 3.5-fold activation of AP-1 respectively (P<0.05). If the cells had been made quiescent, treatment with triptorelin (100 nM) resulted in a 41.7-fold and 48.6-fold increase of AP-1 activation respectively (P<0.001). This effect was completely blocked by simultaneous treatment with pertussis toxin (PTX). A 17.6-fold and 17.3-fold increase of c-jun mRNA expression respectively (P<0.001) was obtained after 20 min of stimulation with triptorelin (100 nM). Treatment with 1 nM triptorelin resulted in a 12.5-fold or an 11.9-fold increase, and treatment with 10 pM triptorelin resulted in a 6.5-fold or a 5.2-fold increase of maximal c-jun mRNA expression respectively (P<0.001). Maximal c-Jun phosphorylation (68.5-fold and 60.2-fold, respectively, P<0.001) was obtained after 90 min incubation with triptorelin (100 nM). CONCLUSIONS: These results suggest that the LHRH agonist triptorelin stimulates the activity of AP-1 in human endometrial cancer cells mediated through PTX-sensitive G-protein alphai. In addition, triptorelin activates JNK, known to activate AP-1. In earlier investigations we have shown that triptorelin does not activate phospholipase and protein kinase C (PKC) in endometrial cancer cells. In addition, it has been demonstrated that triptorelin inhibits growth factor-induced mitogen activated protein kinase (MAPK, ERK) activity. Thus triptorelin-induced activation of the JNK/AP-1 pathway in endometrial cancer cells is independent of the known AP-1 activators, PKC or MAPK (ERK).

Cisplatin increases B-cell-lymphoma-2 expression via activation of protein kinase C and Akt2 in endometrial cancer cells

2011 ◽  
Vol 130 (8) ◽  
pp. 1755-1767 ◽  
Author(s):  
Alexandre Rouette ◽  
Sophie Parent ◽  
Julie Girouard ◽  
Valérie Leblanc ◽  
Eric Asselin
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
B Cell ◽  
Cancer Cells ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Kinase C

scholarly journals Protein kinase C alpha-dependent signaling mediates endometrial cancer cell growth and tumorigenesis

2009 ◽  
Vol 125 (11) ◽  
pp. 2556-2564 ◽  
Author(s):  
James M. Haughian ◽  
Elaine M. Reno ◽  
Alicia M. Thorne ◽  
Andrew P. Bradford
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Kinase C ◽  
Protein Kinase C Alpha

Protein Kinase C Alpha Expression Is Inversely Related to ER Status in Endometrial Carcinoma: Possible Role in AP-1-Mediated Proliferation of ER-Negative Endometrial Cancer

2001 ◽  
Vol 81 (3) ◽  
pp. 366-372 ◽  
Author(s):  
David B. Fournier ◽  
Michael Chisamore ◽  
John R. Lurain ◽  
Alfred W. Rademaker ◽  
V.Craig Jordan ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Endometrial Carcinoma ◽  
Kinase C ◽  
Protein Kinase C Alpha ◽  
Er Status

scholarly journals Effect of protein kinase C alpha, caspase-3, and survivin on apoptosis of oral cancer cells induced by staurosporine1

2005 ◽  
Vol 26 (11) ◽  
pp. 1365-1372 ◽  
Author(s):  
Yu-xia ZHANG ◽  
Shi-bin YU ◽  
Jing-ping OU-YANG ◽  
Dong XIA ◽  
Min WANG ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Kinase C ◽  
Protein Kinase C Alpha ◽  
Oral Cancer Cells

Abstract 4211: Protein kinase C alpha (PKCα) signaling in endometrial cancer

2014 ◽  
Author(s):  
Alice H. Hsu ◽  
Kathryn J. Curry ◽  
Kang-Sup Shim ◽  
Peter Frederick ◽  
Carl D. Morrison ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase C ◽  
Protein Kinase C Alpha

Abstract 4720: Protein kinase C alpha (PKCα) regulates PI3K/AKT signaling in endometrial cancer

2015 ◽  
Author(s):  
Alice H. Hsu ◽  
Kathryn J. Curry ◽  
Kang-Sup Shim ◽  
Peter Frederick ◽  
Carl Morrison ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Akt Signaling ◽  
Kinase C ◽  
Protein Kinase C Alpha
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