ArticleCancer biology & therapy2013
Brk/PTK6 cooperates with HER2 and Src in regulating breast cancer cell survival and epithelial-to-mesenchymal transition.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- A PROTAC degrader suppresses oncogenic functions of PTK6, inducing apoptosis of breast cancer cells.Cell chemical biology · 2025Article
- Immunomagnetic Isolation of HER2-Positive Breast Cancer Cells Using a Microfluidic Device.ACS omega · 2023Article
- Epigenetic Deregulation of Protein Tyrosine Kinase 6 Promotes Carcinogenesis of Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2022Article
- Epithelial-to-Mesenchymal Transition Signaling Pathways Responsible for Breast Cancer Metastasis.Cellular and molecular bioengineering · 2022Review
- Review
- Consequences of EMT-Driven Changes in the Immune Microenvironment of Breast Cancer and Therapeutic Response of Cancer Cells.Journal of clinical medicine · 2019Review
- Taxol Induces Brk-dependent Prosurvival Phenotypes in TNBC Cells through an AhR/GR/HIF-driven Signaling Axis.Molecular cancer research : MCR · 2018Article
- Breast Tumor Kinase (Brk/PTK6) Is Induced by HIF, Glucocorticoid Receptor, and PELP1-Mediated Stress Signaling in Triple-Negative Breast Cancer.Cancer research · 2016Article
- PTK6 promotes hepatocellular carcinoma cell proliferation and invasion.American journal of translational research · 2016Article
- Protein tyrosine kinase 6 promotes ERBB2-induced mammary gland tumorigenesis in the mouse.Cell death & disease · 2015Article
- Hyaluronan expression in primary and secondary brain tumors.Annals of translational medicine · 2015Article
- Sphingosine-1-phosphate induces the migration of thyroid follicular carcinoma cells through the microRNA-17/PTK6/ERK1/2 pathway.PloS one · 2015Article
- PTK6/BRK is expressed in the normal mammary gland and activated at the plasma membrane in breast tumors.Oncotarget · 2014Article
- Isolation of breast cancer and gastric cancer circulating tumor cells by use of an anti HER2-based microfluidic device.Lab on a chip · 2014Article
- Article
- Pathways driving the endocytosis of mutant and wild-type EGFR in cancer.Oncoscience · 2014Article
- Article
- Breast tumor kinase (Brk/PTK6) is a mediator of hypoxia-associated breast cancer progression.Cancer research · 2013Article
- HER2 regulates Brk/PTK6 stability via upregulating calpastatin, an inhibitor of calpain.Cellular signalling · 2013Article
- HDACIs and the inhibition of invasive potential.Cancer biology & therapy · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Breast tumor kinase (Brk)/protein tyrosine kinase-6 (PTK-6) is a nonreceptor PTK commonly expressed at high levels in breast cancer. Brk interacts closely with members of the human epidermal growth factor receptor (HER) family in breast cancer but the functional role of this interaction remains to be determined. Here, we provide novel mechanistic insights into the role of Brk in regulating cell survival and epithelial-to-mesenchymal transition (EMT) in the context of HER2-positive breast cancer cells. Overexpression of HER2 in MCF7 breast cancer cells (MCF7HER2) led to a higher level of Brk protein and concomitantly reduced Src Y416-phosphorylation, and the cells became mesenchymal in morphology. An in vivo selection of MCF7HER2 cells in nude mice resulted in a subline, termed EMT1, that exhibited not only mesenchymal morphology but also enhanced migration potential. Compared with MCF7HER2 cells, EMT1 cells maintained a similar level of HER2 protein but had much higher level of activated HER2, and the increase in Brk protein and the decrease in Src Y416-phosphorylation were less in EMT1 cells. EMT1 cells exhibited increased sensitivity to both pharmacological inhibition of HER2 and knockdown of Brk than did MCF7HER2 cells. Knockdown of Brk induced apoptosis and partially reversed the EMT phenotype in EMT1 cells. Overexpression of a constitutively active STAT3, a known substrate of Brk, overcame Brk knockdown-induced effects in EMT1 cells. Together, our findings support a new paradigm wherein Brk plays both a complementary and a counterbalancing role in cooperating with HER2 and Src to regulate breast cancer cell survival and EMT.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.