ArticleCell cycle (Georgetown, Tex.)2010
Cytoplasmic retention of protein tyrosine kinase 6 promotes growth of prostate tumor cells.
Article in Cell cycle (Georgetown, Tex.), 2010. 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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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Protein tyrosine kinase-6 is post-translationally regulated by arginine methylation and ubiquitination.Cell death & disease · 2026Article
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- Review
- Targeting protein tyrosine kinase 6 in cancer.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- Protein tyrosine kinase 6 signaling in prostate cancer.American journal of clinical and experimental urology · 2020Review
- Vemurafenib Inhibits Active PTK6 inMolecular cancer therapeutics · 2019Article
- PTEN is a protein phosphatase that targets active PTK6 and inhibits PTK6 oncogenic signaling in prostate cancer.Nature communications · 2017Article
- Sam68 is Overexpressed in Epithelial Ovarian Cancer and Promotes Tumor Cell Proliferation.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Protein Tyrosine Kinase 6 Regulates UVB-Induced Signaling and Tumorigenesis in Mouse Skin.The Journal of investigative dermatology · 2015Article
- Downregulated expression of PTK6 is correlated with poor survival in esophageal squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2014Article
- HIF-1α-independent hypoxia-induced rapid PTK6 stabilization is associated with increased motility and invasion.Cancer biology & therapy · 2014Article
- PTK6/BRK is expressed in the normal mammary gland and activated at the plasma membrane in breast tumors.Oncotarget · 2014Article
- BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.PloS one · 2014Article
- Article
- Protein tyrosine kinase 6 protects cells from anoikis by directly phosphorylating focal adhesion kinase and activating AKT.Oncogene · 2013Article
- PTK6 activation at the membrane regulates epithelial-mesenchymal transition in prostate cancer.Cancer research · 2013Article
- Context-specific protein tyrosine kinase 6 (PTK6) signalling in prostate cancer.European journal of clinical investigation · 2013Review
- Low expression of PTK6/Brk predicts poor prognosis in patients with laryngeal squamous cell carcinoma.Journal of translational medicine · 2013Article
- Targeting protein tyrosine kinase 6 enhances apoptosis of colon cancer cells following DNA damage.Molecular cancer therapeutics · 2012Article
- Protein-tyrosine kinase 6 promotes peripheral adhesion complex formation and cell migration by phosphorylating p130 CRK-associated substrate.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Protein tyrosine kinase 6 (PTK6) is an intracellular tyrosine kinase that is nuclear in epithelial cells of the normal prostate, but cytoplasmic in prostate tumors and in the PC3 prostate tumor cell line. The impact of altered PTK6 intracellular localization in prostate tumor cells has not been extensively explored. Knockdown of endogenous cytoplasmic PTK6 resulted in decreased PC3 cell proliferation and colony formation, suggesting that cytoplasmic PTK6 stimulates oncogenic pathways. In contrast, reintroduction of PTK6 into nuclei of PC3 cells had a negative effect on growth. Enhanced tyrosine phosphorylation of the PTK6 substrate Sam68 was detected in cells expressing nuclear-targeted PTK6. We found that mechanisms regulating nuclear localization of PTK6 are intact in PC3 cells. Transiently overexpressed PTK6 readily enters the nucleus. Ectopic expression of ALT-PTK6, a catalytically inactive splice variant of PTK6, did not affect localization of endogenous PTK6 in PC3 cells. Using leptomycin B, we confirmed that cytoplasmic localization of endogenous PTK6 is not due to Crm-1/exportin-1 mediated nuclear export. In addition, overexpression of the PTK6 nuclear substrate Sam68 is not sufficient to bring PTK6 into the nucleus. While exogenous PTK6 was readily detected in the nucleus when transiently expressed at high levels, low-level expression of inducible wild type PTK6 in stable cell lines resulted in its cytoplasmic retention. Our results suggest that retention of PTK6 in the cytoplasm of prostate cancer cells disrupts its ability to regulate nuclear substrates and leads to aberrant growth. In prostate cancer, restoring PTK6 nuclear localization may have therapeutic advantages.
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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.