Effect of protein tyrosine phosphatase 1B expression on transformation by the human neu oncogene

Many oncogenes encode proteins with a tyrosine kinase activity that appears to be directly involved in the process of transformation. Because these kinases are themselves activated for transformation by tyrosine phosphorylation, proteins which remove phosphate from tyrosine residues, protein tyrosin...

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Published inCancer research (Chicago, Ill.) Vol. 52; no. 2; pp. 478 - 482
Main Authors BROWN-SHIMER, S, JOHNSON, K. A, HILL, D. E, BRUSKIN, A. M
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Association for Cancer Research 15.01.1992
Subjects
3T3 Cells - enzymology
Animals
Biological and medical sciences
Cell Division
Cell metabolism, cell oxidation
Cell physiology
Cell Transformation, Neoplastic - metabolism
Fundamental and applied biological sciences. Psychology
genes
Genes, Tumor Suppressor
Humans
Mice
Molecular and cellular biology
neu
NIH 3T3 cells
Oncogenes
Protein Tyrosine Phosphatase, Non-Receptor Type 1
Protein Tyrosine Phosphatases - metabolism
protein-tyrosine-phosphatase
Proto-Oncogene Proteins - genetics
Receptor, ErbB-2
Transfection
transformation
Phosphorylation
Enzyme
Rodentia
Tumorigenicity
Gene expression
In vitro
Genetic transfer
Vertebrata
Mammalia
Mouse
Animal
Malignant transformation
Inhibition
Onc gene
Protein-tyrosine-phosphatase
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Summary:Many oncogenes encode proteins with a tyrosine kinase activity that appears to be directly involved in the process of transformation. Because these kinases are themselves activated for transformation by tyrosine phosphorylation, proteins which remove phosphate from tyrosine residues, protein tyrosine phosphatases (also termed phosphotyrosine phosphatases and protein phosphotyrosyl phosphatases), are intuitive candidate transformation suppressors. The human PTP1B gene, previously cloned in our laboratory and encoding the low molecular weight protein tyrosine phosphatase PTPase 1B, was introduced into NIH 3T3 cells. Subsequent transformation of these PTPase 1B-expressing cells by an oncogenic form of the human neu gene was suppressed relative to control NIH 3T3 cells. This suppression of transformation was observed in assays for focus formation, anchorage-independent growth, and tumorigenicity. Tumorigenicity assays indicated a complex effect of PTPase 1B expression on transformation.
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ISSN:0008-5472
1538-7445