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Expression and tyrosine phosphorylation of EMS1 in human breast cancer cell lines
Author(s) -
Campbell Douglas H.,
deFazio Anna,
Sutherland Robert L.,
Daly Roger J.
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19961115)68:4<485::aid-ijc14>3.0.co;2-4
Subject(s) - phosphorylation , breast cancer , human breast , tyrosine phosphorylation , cancer research , tyrosine , cancer , biology , medicine , oncology , pathology , genetics , biochemistry
The EMS 1 gene encodes an 80/85 kDa c‐src substrate and localises with the CCND 1 gene to chromosome 11q13. This locus is amplified in approximately 13% of human breast cancers. EMS 1 gene amplification and expression were characterised in a panel of human breast cancer cell lines to determine at what levels expression is regulated. The degree of tyrosine phosphorylation of EMS 1 protein was also determined and compared with the activity of src‐family kinases. The EMS 1 gene was amplified in 6 of 20 cell lines investigated: MDA‐MB‐134, ‐157, ‐175, ‐453, ZR‐75‐1 and MCF‐7. In the MDA‐MB‐157 and MCF‐7 cell lines, EMS 1 was amplified in the absence of CCND 1 gene amplification. EMS1 protein levels were increased relative to normal breast epithelial cells in 6 cell lines (ZR‐75‐1, MDA‐MB‐134, ‐175, ‐453, MCF‐7 and BT‐474). Of these, BT‐474 is the only cell line that does not exhibit EMS 1 amplification or increased EMS1 mRNA levels. EMS 1 tyrosine phosphorylation was 3‐fold higher in BT‐474 and T‐47D cells, which exhibited relatively high total src activity coupled with expression of both c‐fyn and c‐yes, than in MDA‐MB‐453 cells, which expressed only c‐yes. Our results therefore demonstrate gene amplification to be the predominant mechanism underlying EMS1 over‐expression in human breast cancer cell lines and identify tyrosine phosphorylation as a further level at which regulation of this protein may be perturbed. © 1996 Wiley‐Liss, Inc.