ArticleCancer research2010
Compensatory upregulation of tyrosine kinase Etk/BMX in response to androgen deprivation promotes castration-resistant growth of prostate cancer cells.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 64 citations in OpenAlex.
- Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Discovery of Dihydropyrimido-Pyrimidine-Based Bone Marrow Tyrosine Kinase Gene in Chromosome X Protein Proteolysis-Targeting Chimeras for the Treatment of Prostate Cancer.ACS medicinal chemistry letters · 2026Article
- HSD3B1, prostate cancer mortality and modifiable outcomes.Nature reviews. Urology · 2025Review
- Molecular landscape for risk prediction and personalized therapeutics of castration-resistant prostate cancer: at a glance.Frontiers in endocrinology · 2024Review
- Emerging proteins involved in castration‑resistant prostate cancer via the AR‑dependent and AR‑independent pathways (Review).International journal of oncology · 2023Review
- Deregulated kinase action in prostate cancer: molecular basis and therapeutic implications.Endocrine-related cancer · 2023Review
- A phosphorylation switch controls androgen biosynthesis in prostate cancer.The Journal of clinical investigation · 2023Article
- BMX controls 3βHSD1 and sex steroid biosynthesis in cancer.The Journal of clinical investigation · 2023Article
- Saracatinib synergizes with enzalutamide to downregulate AR activity in CRPC.Frontiers in oncology · 2023Article
- A scalable insect cell-based production process of the human recombinant BMX for in-vitro covalent ligand high-throughput screening.Bioprocess and biosystems engineering · 2021Article
- Emerging Kinase Therapeutic Targets in Pancreatic Ductal Adenocarcinoma and Pancreatic Cancer Desmoplasia.International journal of molecular sciences · 2020Review
- Structural and biophysical insights into the mode of covalent binding of rationally designed potent BMX inhibitors.RSC chemical biology · 2020Article
- Loss of a Negative Feedback Loop between IRF8 and AR Promotes Prostate Cancer Growth and Enzalutamide Resistance.Cancer research · 2020Article
- New targets for therapy: antigen identification in adults with B-cell acute lymphoblastic leukaemia.Cancer immunology, immunotherapy : CII · 2020Review
- Nuclear localization of the tyrosine kinase BMX mediates VEGFR2 expression.Journal of cellular and molecular medicine · 2020Article
- Induction of entosis in prostate cancer cells by nintedanib and its therapeutic implications.Oncology letters · 2019Article
- BMX-Mediated Regulation of Multiple Tyrosine Kinases Contributes to Castration Resistance in Prostate Cancer.Cancer research · 2018Article
- Disruption of MEK/ERK/c-Myc signaling radiosensitizes prostate cancer cells in vitro and in vivo.Journal of cancer research and clinical oncology · 2018Article
- Hypoxia-induced upregulation of BMX kinase mediates therapeutic resistance in acute myeloid leukemia.The Journal of clinical investigation · 2018Article
- Targeting Glioma Stem Cell-Derived Pericytes Disrupts the Blood-Tumor Barrier and Improves Chemotherapeutic Efficacy.Cell stem cell · 2017Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously showed that targeted expression of non-receptor tyrosine kinase Etk/BMX in mouse prostate induces prostate intraepithelial neoplasia, implying a possible causal role of Etk in prostate cancer development and progression. Here, we report that Etk is upregulated in both human and mouse prostates in response to androgen ablation. Etk expression seems to be differentially regulated by androgen and interleukin 6 (IL-6), which is possibly mediated by the androgen receptor (AR) in prostate cancer cells. Our immunohistochemical analysis of tissue microarrays containing 112 human prostate tumor samples revealed that Etk expression is elevated in hormone-resistant prostate cancer and positively correlated with tyrosine phosphorylation of AR (Pearson correlation coefficient rho = 0.71, P < 0.0001). AR tyrosine phosphorylation is increased in Etk-overexpressing cells, suggesting that Etk may be another tyrosine kinase, in addition to Src and Ack-1, which can phosphorylate AR. We also showed that Etk can directly interact with AR through its Src homology 2 domain, and such interaction may prevent the association of AR with Mdm2, leading to stabilization of AR under androgen-depleted conditions. Overexpression of Etk in androgen-sensitive LNCaP cells promotes tumor growth while knocking down Etk expression in hormone-insensitive prostate cancer cells by a specific shRNA that inhibits tumor growth under androgen-depleted conditions. Taken together, our data suggest that Etk may be a component of the adaptive compensatory mechanism activated by androgen ablation in prostate and may play a role in hormone resistance, at least in part, through direct modulation of the AR signaling pathway.
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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.