Document Detail


Autocrine human growth hormone enhancement of human mammary carcinoma cell spreading is Jak2 dependent.
MedLine Citation:
PMID:  10746665     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We investigated the role of autocrine production of human (h) GH in the attachment and spreading of mammary carcinoma cells in vitro. We used a previously described model system for the study of the autocrine/paracrine role of GH in which the hGH gene (MCF-hGH) or a translation-deficient hGH gene (MCF-MUT) was stably transfected into MCF-7 cells. No differences in attachment to a collagen matrix between MCF-hGH and MCF-MUT cells were observed in either serum-free medium (SFM) or medium containing exogenous hGH, 5% serum, or 10% serum. In contrast, MCF-hGH cells spread more rapidly on a collagen matrix than did MCF-MUT cells. Exogenous hGH and 10% serum interacted with autocrine production of hGH in an additive manner to increase cell spreading. MCF-hGH cells formed filipodia and stress fibers earlier than MCF-MUT cells during the process of cell spreading and possessed marked differences in morphology after spreading. MCF-MUT cells displayed uniform and symmetrical formation of stress fibers, whereas MCF-hGH cells displayed irregular and elongated stress fiber formation. The level of cytoplasmic phosphotyrosine was increased in MCF-hGH compared with MCF-MUT cells during spreading and displayed colocalization with Janus kinase 2 (JAK2). Basal JAK2 tyrosine phosphorylation was increased, and it increased further on spreading in MCF-hGH cells compared with MCF-MUT cells. Transient transfection of JAK2 complementary DNA resulted in interaction with autocrine hGH to increase the rate of cell spreading in MCF-hGH cells compared with MCF-MUT cells. Treatment with a selective JAK2 tyrosine kinase inhibitor (AG 490) reduced the rate of MCF-hGH cell spreading to the rate of MCF-MUT cell spreading. Thus, we conclude that autocrine production of hGH enhances the rate of mammary carcinoma cell spreading in a JAK2-dependent manner.
Authors:
K K Kaulsay; H C Mertani; K O Lee; P E Lobie
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Endocrinology     Volume:  141     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2000 Apr 
Date Detail:
Created Date:  2000-04-11     Completed Date:  2000-04-11     Revised Date:  2012-06-05    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1571-84     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, National University of Singapore, Republic of Singapore.
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MeSH Terms
Descriptor/Qualifier:
Actins / physiology
Autocrine Communication / physiology*
Breast Neoplasms / pathology*,  physiopathology
Carcinoma / pathology*,  physiopathology
Cell Adhesion
Enzyme Inhibitors / pharmacology
Female
Growth Hormone / analogs & derivatives,  pharmacology
Hormone Antagonists / pharmacology
Human Growth Hormone / physiology*
Humans
Janus Kinase 2
Phosphorylation
Phosphotyrosine / metabolism
Protein-Tyrosine Kinases / antagonists & inhibitors,  metabolism,  physiology*
Proto-Oncogene Proteins*
Receptors, Somatotropin / antagonists & inhibitors
Recombinant Proteins*
Tissue Distribution
Tumor Cells, Cultured / physiology
Tyrosine / metabolism
Tyrphostins / pharmacology
Chemical
Reg. No./Substance:
0/Actins; 0/Enzyme Inhibitors; 0/G120R protein, human; 0/Hormone Antagonists; 0/Proto-Oncogene Proteins; 0/Receptors, Somatotropin; 0/Recombinant Proteins; 0/Tyrphostins; 0/alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 12629-01-5/Human Growth Hormone; 21820-51-9/Phosphotyrosine; 55520-40-6/Tyrosine; 9002-72-6/Growth Hormone; EC 2.7.10.1/Janus Kinase 2; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.2/JAK2 protein, human

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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