Cardiac hormones are c-Jun-N-Terminal Kinase 2-inhibiting peptides

No Thumbnail Available
Authors
Lane, Meghan L.
Santana, Omar
Frost, Chelsea D.
Nguyen, Jennifer P.
Guerrero, Jennifer
Skelton, William P.
Skelton, Michelle
Vesely, David L.
Advisors
Issue Date
2012-03
Type
Article
Keywords
c-Jun-N-terminal kinase 2 (JNK2) , Mitogen-activated protein kinase 9 (MAPK9) , Stress-activated protein kinase 1 alpha (SAPK1α) , Natriuretic hormones , Cardiac hormones
Research Projects
Organizational Units
Journal Issue
Citation
Lane M.L., Santana O., Frost C.D., Guerrero J., Skelton M., et al. 2012. "Cardiac hormones are c-Jun-N-terminal kinase 2-inhibiting peptides". Anticancer Research. 32 (3): 721-725
Abstract

Background: Four cardiac peptide hormones, namely vessel dilator, long-acting natriuretic peptide (LANP), kaliuretic peptide, and atrial natriuretic peptide (ANP) have anticancer effects. Materials and Methods: The effects of these four cardiac hormones on human c-Jun-N-terminal kinase 2 (JNK2) were examined in human small cell lung cancer and human prostate cancer cells. Results: Vessel dilator, LANP, kaliuretic peptide and ANP maximally reduced expression of JNK2 by 89%, 56%, 45%, and 28%, respectively (each at p<0.0001) in human small cell lung cancer cells. In human prostate adenocarcinoma cells, JNK2 was maximally decreased 76%, 56%, 45%, (each at p<0.0001), and 28% (p<0.01) secondary to vessel dilator, LANP, kaliuretic peptide and ANP, respectively. Conclusion: These results indicate that four cardiac hormones are significant inhibitors (by up to 89%) of JNK2 in human small cell lung cancer cells and up to 76% in human prostate adenocarcinoma cells as part of their anticancer mechanism(s) of action.

Table of Contents
Description
Full text of this article is not available in SOAR.
Publisher
International Institute of Anticancer Research
Journal
Book Title
Series
Anticancer Research;2012:, v.32, no.3
PubMed ID
DOI
ISSN
0250-7005
1791-7530
EISSN