rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
1
|
pubmed:dateCreated |
1998-4-2
|
pubmed:abstractText |
MDA-468 human breast cancer cells overexpress the EGFR and exhibit a functional TGFalpha-EGFR autocrine pathway. Loss of EGFR expression following stable transfection with an antisense EGFR cDNA containing plasmid down-regulates type I cAMP-dependent protein kinase (PKAI) expression with acquisition of cell growth resistance to the PKAI inhibitor 8-Cl-cAMP. These results suggest that PKAI expression and function are controlled by a TGFalpha-EGFR autocrine pathway in human breast cancer cells overexpressing the EGFR.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
0167-6806
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
47
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
57-62
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:9493976-8-Bromo Cyclic Adenosine Monophosphate,
pubmed-meshheading:9493976-Breast Neoplasms,
pubmed-meshheading:9493976-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:9493976-DNA, Antisense,
pubmed-meshheading:9493976-Down-Regulation,
pubmed-meshheading:9493976-Female,
pubmed-meshheading:9493976-Humans,
pubmed-meshheading:9493976-Receptor, Epidermal Growth Factor,
pubmed-meshheading:9493976-Transfection,
pubmed-meshheading:9493976-Transforming Growth Factor alpha,
pubmed-meshheading:9493976-Tumor Cells, Cultured
|
pubmed:year |
1998
|
pubmed:articleTitle |
Down-regulation of type I protein kinase A by transfection of human breast cancer cells with an epidermal growth factor receptor antisense expression vector.
|
pubmed:affiliation |
Dipartimento di Endocrinologia e Oncologia Molecolare e Clinica, Facoltà di Medicina e Chirurgia, Università degli Studi di Napoli Federico II, Italy.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|