Document Detail


Contrasting morphological changes in PC12 flat cells expressing two different forms of exogenous oncogenic ras.
MedLine Citation:
PMID:  8125159     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oncogenic ras is known to transform certain cells, whereas it induces terminal differentiation of others, e.g., neuronal differentiation of PC12 cells. MPT1 is a PC12 flat cell variant that extends glial-like processes and exhibits some properties of noncancer cells in culture, e.g., absence of anchorage-independent growth. Expression of oncogenic ras by MPT1 cells failed to result in neuronal differentiation, but such cells exhibited two contrasting morphological changes under certain conditions. First, they retained their extended processes in the presence of dexamethasone, unlike MPT1 cells not expressing oncogenic ras. Second, confluent cultures of ras-expressing MPT1 cells contained foci of transformed-looking cells that were refractile and grew in multiple layers. Thus, ras seemed to induce both a kind of differentiation and transformation of MPT1 cells. MPT1 cells were transfected with a plasmid carrying an oncogenic Harvey ras gene under transcriptional control of the metallothionein promoter. Two subclones of the transfected cells exhibited different responses to the induction of ras and expressed two different forms of the ras gene product. One clone extended dexamethasone-resistant processes and the second clone exhibited a more transformed phenotype. The ras gene product expressed in these two clones differed in migration on sodium dodecyl sulfate-polyacrylamide gel electrophoresis and in the extent of phosphorylation. These results suggest that ras protein phosphorylation may be important in determining whether a ras-mediated response is differentiation or transformation.
Authors:
Y Y Rozenberg; B D Howard
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Experimental cell research     Volume:  211     ISSN:  0014-4827     ISO Abbreviation:  Exp. Cell Res.     Publication Date:  1994 Mar 
Date Detail:
Created Date:  1994-04-12     Completed Date:  1994-04-12     Revised Date:  2012-06-01    
Medline Journal Info:
Nlm Unique ID:  0373226     Medline TA:  Exp Cell Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  59-67     Citation Subset:  IM    
Affiliation:
Department of Biological Chemistry, School of Medicine, University of California, Los Angeles 90024.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cadmium / pharmacology
Cell Adhesion / physiology
Cloning, Molecular
DNA, Neoplasm / analysis,  genetics
Dexamethasone / pharmacology
Electrophoresis, Polyacrylamide Gel
Gene Expression Regulation, Neoplastic / genetics
Genes, ras / genetics
Genetic Variation
Glial Fibrillary Acidic Protein / analysis,  metabolism
Kirsten murine sarcoma virus / genetics
Lovastatin / pharmacology
Oncogene Protein p21(ras) / analysis*,  genetics,  metabolism
Oncogene Proteins, Viral / genetics,  metabolism,  physiology*
PC12 Cells / chemistry*
Phenotype
Phosphorylation
Proto-Oncogene Proteins*
RNA, Messenger / analysis,  genetics
S100 Proteins / analysis,  metabolism
Transfection
src-Family Kinases
Grant Support
ID/Acronym/Agency:
MH09736/MH/NIMH NIH HHS; MH38633/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/DNA, Neoplasm; 0/Glial Fibrillary Acidic Protein; 0/Oncogene Proteins, Viral; 0/Proto-Oncogene Proteins; 0/RNA, Messenger; 0/S100 Proteins; 50-02-2/Dexamethasone; 7440-43-9/Cadmium; 75330-75-5/Lovastatin; EC 2.7.10.2/proto-oncogene proteins c-fgr; EC 2.7.10.2/src-Family Kinases; EC 3.6.5.2/Oncogene Protein p21(ras)

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


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