Role of c-Src and focal adhesion kinase in progression and metastasis of estrogen receptor-positive breast cancer
The non-receptor tyrosine kinases c-Src and focal adhesion kinase (Fak) mediate signal transduction pathways that regulate cell proliferation, survival, invasion, and metastasis. Here, we investigated whether c-Src and Fak are activated during progression of hormone-dependent breast cancer. Maximall...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2006-03, Vol.341 (1), p.73-81 |
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| creator | Planas-Silva, Maricarmen D. Bruggeman, Richard D. Grenko, Ronald T. Stanley Smith, J. |
| description | The non-receptor tyrosine kinases c-Src and focal adhesion kinase (Fak) mediate signal transduction pathways that regulate cell proliferation, survival, invasion, and metastasis. Here, we investigated whether c-Src and Fak are activated during progression of hormone-dependent breast cancer. Maximally active c-Src was overexpressed in a subset of tamoxifen-resistant variants and in metastases of recurrent hormone-treated breast cancer. Active Fak was also frequently observed in these tumors. We also show that estrogen receptor (ER) can bind to Fak and that estrogen can modulate Fak autophosphorylation supporting a cross-talk between these two pathways. Inhibition of c-Src activity blocked proliferation of all tamoxifen-resistant variants, suggesting that inhibitors of c-Src–Fak activity may delay or prevent progression and metastasis of ER-positive tumors. These studies also raise the possibility that fully active forms of c-Src and Fak in breast tumors may be biomarkers to predict tamoxifen resistance and/or risk of recurrence in ER-positive breast cancer. |
| doi_str_mv | 10.1016/j.bbrc.2005.12.164 |
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Here, we investigated whether c-Src and Fak are activated during progression of hormone-dependent breast cancer. Maximally active c-Src was overexpressed in a subset of tamoxifen-resistant variants and in metastases of recurrent hormone-treated breast cancer. Active Fak was also frequently observed in these tumors. We also show that estrogen receptor (ER) can bind to Fak and that estrogen can modulate Fak autophosphorylation supporting a cross-talk between these two pathways. Inhibition of c-Src activity blocked proliferation of all tamoxifen-resistant variants, suggesting that inhibitors of c-Src–Fak activity may delay or prevent progression and metastasis of ER-positive tumors. 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Here, we investigated whether c-Src and Fak are activated during progression of hormone-dependent breast cancer. Maximally active c-Src was overexpressed in a subset of tamoxifen-resistant variants and in metastases of recurrent hormone-treated breast cancer. Active Fak was also frequently observed in these tumors. We also show that estrogen receptor (ER) can bind to Fak and that estrogen can modulate Fak autophosphorylation supporting a cross-talk between these two pathways. Inhibition of c-Src activity blocked proliferation of all tamoxifen-resistant variants, suggesting that inhibitors of c-Src–Fak activity may delay or prevent progression and metastasis of ER-positive tumors. These studies also raise the possibility that fully active forms of c-Src and Fak in breast tumors may be biomarkers to predict tamoxifen resistance and/or risk of recurrence in ER-positive breast cancer.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>BIOLOGICAL MARKERS</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast Neoplasms - secondary</subject><subject>c-Src tyrosine kinase</subject><subject>Cell Line, Tumor</subject><subject>CELL PROLIFERATION</subject><subject>Disease Progression</subject><subject>Enzyme Activation</subject><subject>Estrogen</subject><subject>Estrogen receptor</subject><subject>ESTROGENS</subject><subject>Focal adhesion kinase</subject><subject>Focal Adhesion Protein-Tyrosine Kinases - metabolism</subject><subject>Humans</subject><subject>INHIBITION</subject><subject>MAMMARY GLANDS</subject><subject>METASTASES</subject><subject>Metastasis</subject><subject>Neoplasm Proteins - metabolism</subject><subject>NEOPLASMS</subject><subject>PHOSPHOTRANSFERASES</subject><subject>Proto-Oncogene Proteins pp60(c-src) - metabolism</subject><subject>RECEPTORS</subject><subject>Receptors, Estrogen - metabolism</subject><subject>TAMOXIFEN</subject><subject>Tamoxifen resistance</subject><subject>Tumor biomarker</subject><subject>TYROSINE</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU-LFDEQxYMo7uzqF_AgAcFbt1Xp6aQDXmRRV1gQ_APeQjqpuBl7OrNJz4Lf3rQz4E0oCFR-9ah6j7EXCC0Cyje7dhyzawVA36JoUW4fsQ2ChkYgbB-zDQDIRmj8ccEuS9kBIG6lfsouKoqiG2DD7r-kiXgK3DVfs-N29jwkZydu_R2VmGb-K862EI8zP-T0M1P5213BPS221IplFaCy1H-aeSZHhyXl5pBKXOID8TFTBbmzs6P8jD0Jdir0_Pxese8f3n-7vmluP3_8dP3utnHdIJZGawqqF2hx0NSr0HVehyD9YAfVwWhRKBzJCiWlkxBGQVp52PZKeQvBy-6KvTrpprJEU1xcyN25NM_kFiNA6WEQUKnXJ6oed3-sN5h9LI6myc6UjsUoUAAD9hUUJ9DlVEqmYA457m3-bRDMGofZmTUOs8ZhUJjqcR16eVY_jnvy_0bO_lfg7Qmg6sRDpLwuStUmH_O6p0_xf_p_AGOynF4</recordid><startdate>20060303</startdate><enddate>20060303</enddate><creator>Planas-Silva, Maricarmen D.</creator><creator>Bruggeman, Richard D.</creator><creator>Grenko, Ronald T.</creator><creator>Stanley Smith, J.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20060303</creationdate><title>Role of c-Src and focal adhesion kinase in progression and metastasis of estrogen receptor-positive breast cancer</title><author>Planas-Silva, Maricarmen D. ; Bruggeman, Richard D. ; Grenko, Ronald T. ; Stanley Smith, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c382t-99ef7521a189e57f33d9ff6d8a8730ba1271bea2766c60fb2e97d04577da0fd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>BIOLOGICAL MARKERS</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast Neoplasms - secondary</topic><topic>c-Src tyrosine kinase</topic><topic>Cell Line, Tumor</topic><topic>CELL PROLIFERATION</topic><topic>Disease Progression</topic><topic>Enzyme Activation</topic><topic>Estrogen</topic><topic>Estrogen receptor</topic><topic>ESTROGENS</topic><topic>Focal adhesion kinase</topic><topic>Focal Adhesion Protein-Tyrosine Kinases - metabolism</topic><topic>Humans</topic><topic>INHIBITION</topic><topic>MAMMARY GLANDS</topic><topic>METASTASES</topic><topic>Metastasis</topic><topic>Neoplasm Proteins - metabolism</topic><topic>NEOPLASMS</topic><topic>PHOSPHOTRANSFERASES</topic><topic>Proto-Oncogene Proteins pp60(c-src) - metabolism</topic><topic>RECEPTORS</topic><topic>Receptors, Estrogen - metabolism</topic><topic>TAMOXIFEN</topic><topic>Tamoxifen resistance</topic><topic>Tumor biomarker</topic><topic>TYROSINE</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Planas-Silva, Maricarmen D.</creatorcontrib><creatorcontrib>Bruggeman, Richard D.</creatorcontrib><creatorcontrib>Grenko, Ronald T.</creatorcontrib><creatorcontrib>Stanley Smith, J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Planas-Silva, Maricarmen D.</au><au>Bruggeman, Richard D.</au><au>Grenko, Ronald T.</au><au>Stanley Smith, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of c-Src and focal adhesion kinase in progression and metastasis of estrogen receptor-positive breast cancer</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2006-03-03</date><risdate>2006</risdate><volume>341</volume><issue>1</issue><spage>73</spage><epage>81</epage><pages>73-81</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The non-receptor tyrosine kinases c-Src and focal adhesion kinase (Fak) mediate signal transduction pathways that regulate cell proliferation, survival, invasion, and metastasis. Here, we investigated whether c-Src and Fak are activated during progression of hormone-dependent breast cancer. Maximally active c-Src was overexpressed in a subset of tamoxifen-resistant variants and in metastases of recurrent hormone-treated breast cancer. Active Fak was also frequently observed in these tumors. We also show that estrogen receptor (ER) can bind to Fak and that estrogen can modulate Fak autophosphorylation supporting a cross-talk between these two pathways. Inhibition of c-Src activity blocked proliferation of all tamoxifen-resistant variants, suggesting that inhibitors of c-Src–Fak activity may delay or prevent progression and metastasis of ER-positive tumors. These studies also raise the possibility that fully active forms of c-Src and Fak in breast tumors may be biomarkers to predict tamoxifen resistance and/or risk of recurrence in ER-positive breast cancer.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16412380</pmid><doi>10.1016/j.bbrc.2005.12.164</doi><tpages>9</tpages></addata></record> |
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| subjects | 60 APPLIED LIFE SCIENCES BIOLOGICAL MARKERS Biomarkers, Tumor - metabolism Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Breast Neoplasms - secondary c-Src tyrosine kinase Cell Line, Tumor CELL PROLIFERATION Disease Progression Enzyme Activation Estrogen Estrogen receptor ESTROGENS Focal adhesion kinase Focal Adhesion Protein-Tyrosine Kinases - metabolism Humans INHIBITION MAMMARY GLANDS METASTASES Metastasis Neoplasm Proteins - metabolism NEOPLASMS PHOSPHOTRANSFERASES Proto-Oncogene Proteins pp60(c-src) - metabolism RECEPTORS Receptors, Estrogen - metabolism TAMOXIFEN Tamoxifen resistance Tumor biomarker TYROSINE |
| title | Role of c-Src and focal adhesion kinase in progression and metastasis of estrogen receptor-positive breast cancer |
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