ReviewInternational journal of biological sciences2014
Androgen receptor activation in castration-recurrent prostate cancer: the role of Src-family and Ack1 tyrosine kinases.
Review in International journal of biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Synergistic targeting strategies for prostate cancer.Nature reviews. Urology · 2025Review
- Mechanistic insights into the effects of Tris-2-butoxyethyl phosphate on multiple cancers using network toxicology and molecular docking.Scientific reports · 2025Article
- SHP2 as a primordial epigenetic enzyme expunges histone H3 pTyr-54 to amend androgen receptor homeostasis.Nature communications · 2024Article
- Review
- Review
- Inhibiting ACK1-mediated phosphorylation of C-terminal Src kinase counteracts prostate cancer immune checkpoint blockade resistance.Nature communications · 2022Article
- Advances in the Current Understanding of the Mechanisms Governing the Acquisition of Castration-Resistant Prostate Cancer.Cancers · 2022Review
- Chronologically modified androgen receptor in recurrent castration-resistant prostate cancer and its therapeutic targeting.Science translational medicine · 2022Article
- Review
- Review
- Therapeutic Targeting of Sunitinib-Induced AR Phosphorylation in Renal Cell Carcinoma.Cancer research · 2018Article
- Blockade of ACK1/TNK2 To Squelch the Survival of Prostate Cancer Stem-like Cells.Scientific reports · 2018Article
- Recent advances on the progressive mechanism and therapy in castration-resistant prostate cancer.OncoTargets and therapy · 2018Review
- Identification of novel Ack1-interacting proteins and Ack1 phosphorylated sites in mouse brain by mass spectrometry.Oncotarget · 2017Article
- AR Signaling and the PI3K Pathway in Prostate Cancer.Cancers · 2017Review
- Src promotes castration-recurrent prostate cancer through androgen receptor-dependent canonical and non-canonical transcriptional signatures.Oncotarget · 2017Article
- High-Content Screening Identifies Src Family Kinases as Potential Regulators of AR-V7 Expression and Androgen-Independent Cell Growth.The Prostate · 2017Article
- Non-Genomic Actions of the Androgen Receptor in Prostate Cancer.Frontiers in endocrinology · 2017Review
- Involvement of Activated Cdc42 Kinase1 in Colitis and Colorectal Neoplasms.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Androgen-glucocorticoid interactions in the era of novel prostate cancer therapy.Nature reviews. Urology · 2016Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is growing appreciation that castration-recurrent prostate cancer (CR-CaP) is driven by the continued expression of androgen receptor (AR). AR activation in CR-CaP through various mechanisms, including AR overexpression, expression of AR splice variants or mutants, increased expression of co-regulator proteins, and by post-translational modification, allows for the induction of AR-regulated genes in response to very low levels of tissue-expressed, so-called intracrine androgens, resulting in pathways that mediate CaP proliferation, anti-apoptosis and oncogenic aggressiveness. The current review focuses on the role played by Src-family (SFK) and Ack1 non-receptor tyrosine kinases in activating AR through direct phosphorylation, respectively, on tyrosines 534 or 267, and how these modifications facilitate progression to CR-CaP. The fact that SFK and Ack1 are central mediators for multiple growth factor receptor signaling pathways that become activated in CR-CaP, especially in the context of metastatic growth in the bone, has contributed to recent therapeutic trials using SFK/Ack1 inhibitors in monotherapy or in combination with antagonists of the AR activation axis.
Indexed as
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What OpenQuestion holds
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.