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LAR‐PTPase cDNA transfection suppression of tumor growth of neu oncogene‐transformed human breast carcinoma cells
Author(s) -
Zhai Yifan,
Wirth Julia,
Kang Sanmao,
Welsch Clifford W.,
Esselman Walter J.
Publication year - 1995
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940140206
Subject(s) - biology , protein tyrosine phosphatase , tyrosine phosphorylation , transfection , cancer research , phosphorylation , tyrosine kinase , microbiology and biotechnology , oncogene , tyrosine , cell culture , signal transduction , cell cycle , cell , biochemistry , genetics
The incidence of amplification of neu oncogene‐encoded protein tyrosine kinase in human breast cancer strongly supports the concept that protein tyrosine phosphorylation and dephosphorylation are key regulatory mechanisms in the proliferation, differentiation, and neoplastic transformation of breast epithelial cells. We examined the potential regulatory role of protein tyrosine phosphatases (a) in the maintenance of cellular tyrosine phosphorylation by the introduction of leukocyte common‐antigen‐related PTPase (LAR‐PTPase) cDNA into a tumorigenic human breast carcinoma cell line that overexpressed p185 neu protein tyrosine kinase. The transfected human breast carcinoma cells expressed elevated levels of LAR‐PTPase as assessed by reverse transcription‐polymerase chain reaction and by analysis of LAR‐PTPase protein. The LAR‐PTPase‐transfected human breast carcinoma cells had a significantly ( P <0.01) slower proliferation rate in vitro than control‐trans‐fected cells. When LAR‐PTPase‐transfected cells were inoculated into athymic nude mice, a consistent and significant ( P <0.05) suppression of tumor growth was observed. These results provide evidence that a specific PTPase, LAR‐PTPase, can play a suppressive regulatory role in the tumor growth of human breast carcinoma cells that overexpress p185 neu protein tyrosine kinase. ©1995 Wiley‐Liss, Inc.