Activation of Src family kinases in Neu-induced mammary tumors correlates with their association with distinct sets of tyrosine phosphorylated proteins in vivo - PubMed (original) (raw)
. 1995 Nov 2;11(9):1801-10.
Affiliations
- PMID: 7478608
Activation of Src family kinases in Neu-induced mammary tumors correlates with their association with distinct sets of tyrosine phosphorylated proteins in vivo
S K Muthuswamy et al. Oncogene. 1995.
Abstract
Overexpression and amplification of the erbB-2 (neu) is thought to play a major role in mammary cancer. Although studies suggest that Neu is directly involved in the genesis of mammary tumors, the molecular mechanism by which Neu induces tumors is not well understood. Recently, we have demonstrated that the activity of c-Src tyrosine kinase is elevated in Neu-induced mammary tumors and this elevated activity correlates with its capacity to physically associate with Neu. To explore whether other members of the c-Src family are activated in these mammary tumors, we measured the in vitro kinase activity of the c-Yes and Fyn kinases in protein extracts derived from mammary tumor tissue and morphological normal adjacent tissue. These analyses revealed that c-Yes kinase activity was elevated in Neu-induced tumors by comparison to the adjacent tissue. By contrast, no significant activation of the Fyn kinase was noted in these tumors. Activation of c-Yes tyrosine kinase correlated with the capacity of c-Yes to associate with Neu in vivo in lysates derived from primary tumor samples. Studies with Rat.2 fibroblasts overexpressing activated Neu revealed that c-Src requires the presence of tyrosine phosphorylated Neu for its ability to interact with Neu in vivo. Moreover, analyses using radiolabeled c-Yes SH2 fusion protein revealed that this interaction is likely occurring in a direct fashion. Although both c-Src and c-Yes kinase associate with Neu in vivo, a tyrosine phosphorylated protein of 89 kd (p89) was found associated with c-Src but not with c-Yes in cell lysates derived from mammary epithelial cells transformed by either Neu or PyV middle T antigen. Furthermore, this tyrosine phosphorylated protein was not detected in c-Src complexes derived from fibroblasts transformed by either Neu or PyV middle T. These observations suggest that p89 associates with c-Src only in mammary epithelial cells and not in fibroblasts.
Similar articles
- Protein tyrosine phosphatase epsilon activates Yes and Fyn in Neu-induced mammary tumor cells.
Granot-Attas S, Elson A. Granot-Attas S, et al. Exp Cell Res. 2004 Mar 10;294(1):236-43. doi: 10.1016/j.yexcr.2003.11.003. Exp Cell Res. 2004. PMID: 14980517 - Induction of tumor formation and cell transformation by polyoma middle T antigen in the absence of Src.
Thomas JE, Aguzzi A, Soriano P, Wagner EF, Brugge JS. Thomas JE, et al. Oncogene. 1993 Sep;8(9):2521-9. Oncogene. 1993. PMID: 7689725 - Protein tyrosine phosphatase epsilon and Neu-induced mammary tumorigenesis.
Berman-Golan D, Granot-Attas S, Elson A. Berman-Golan D, et al. Cancer Metastasis Rev. 2008 Jun;27(2):193-203. doi: 10.1007/s10555-008-9124-0. Cancer Metastasis Rev. 2008. PMID: 18231724 Review. - The p60c-src family of protein-tyrosine kinases: structure, regulation, and function.
Brickell PM. Brickell PM. Crit Rev Oncog. 1992;3(4):401-46. Crit Rev Oncog. 1992. PMID: 1384720 Review.
Cited by
- Role of Epidermal Growth Factor Receptor (EGFR) and Its Ligands in Kidney Inflammation and Damage.
Rayego-Mateos S, Rodrigues-Diez R, Morgado-Pascual JL, Valentijn F, Valdivielso JM, Goldschmeding R, Ruiz-Ortega M. Rayego-Mateos S, et al. Mediators Inflamm. 2018 Dec 23;2018:8739473. doi: 10.1155/2018/8739473. eCollection 2018. Mediators Inflamm. 2018. PMID: 30670929 Free PMC article. Review. - Src Cooperates with Oncogenic Ras in Tumourigenesis via the JNK and PI3K Pathways in Drosophila epithelial Tissue.
Poon CLC, Brumby AM, Richardson HE. Poon CLC, et al. Int J Mol Sci. 2018 May 27;19(6):1585. doi: 10.3390/ijms19061585. Int J Mol Sci. 2018. PMID: 29861494 Free PMC article. - HER2 and uPAR cooperativity contribute to metastatic phenotype of HER2-positive breast cancer.
Indira Chandran V, Eppenberger-Castori S, Venkatesh T, Vine KL, Ranson M. Indira Chandran V, et al. Oncoscience. 2015 Mar 23;2(3):207-24. doi: 10.18632/oncoscience.146. eCollection 2015. Oncoscience. 2015. PMID: 25897424 Free PMC article. Review. - Modulating therapeutic effects of the c-Src inhibitor via oestrogen receptor and human epidermal growth factor receptor 2 in breast cancer cell lines.
Fan P, McDaniel RE, Kim HR, Clagett D, Haddad B, Jordan VC. Fan P, et al. Eur J Cancer. 2012 Dec;48(18):3488-98. doi: 10.1016/j.ejca.2012.04.020. Epub 2012 Jun 2. Eur J Cancer. 2012. PMID: 22658320 Free PMC article. - Oncogenes and tumor suppressor genes.
Lee EY, Muller WJ. Lee EY, et al. Cold Spring Harb Perspect Biol. 2010 Oct;2(10):a003236. doi: 10.1101/cshperspect.a003236. Epub 2010 Aug 18. Cold Spring Harb Perspect Biol. 2010. PMID: 20719876 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources
Research Materials
Miscellaneous