ArticleOncotarget2016
GRK3 is a direct target of CREB activation and regulates neuroendocrine differentiation of prostate cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- Cholesterol metabolism regulated by CAMKK2-CREB signaling promotes castration-resistant prostate cancer.Cell reports · 2025Article
- Androgen deprivation induces neuroendocrine phenotypes in prostate cancer cells through CREB1/EZH2-mediated downregulation of REST.Cell death discovery · 2024Article
- Androgen deprivation induces neuroendocrine phenotypes in prostate cancer cells through CREB1/EZH2-mediated downregulation of REST.Research square · 2023Article
- A novel GRK3-HDAC2 regulatory pathway is a key direct link between neuroendocrine differentiation and angiogenesis in prostate cancer progression.Cancer letters · 2023Article
- Review
- Neuropilin-2 axis in regulating secretory phenotype of neuroendocrine-like prostate cancer cells and its implication in therapy resistance.Cell reports · 2022Article
- Advances in neuroendocrine prostate cancer research: From model construction to molecular network analyses.Laboratory investigation; a journal of technical methods and pathology · 2022Review
- The Role of the CREB Protein Family Members and the Related Transcription Factors in Radioresistance Mechanisms.Life (Basel, Switzerland) · 2021Review
- Pyrrolizidine alkaloid-induced transcriptomic changes in rat lungs in a 28-day subacute feeding study.Archives of toxicology · 2021Article
- Review
- Neuroendocrine cells of the prostate: Histology, biological functions, and molecular mechanisms.Precision clinical medicine · 2021Review
- Review
- Review
- Unraveling the Molecular Nexus between GPCRs, ERS, and EMT.Mediators of inflammation · 2021Review
- GRK2 Suppresses Hepatocellular Carcinoma Metastasis and Invasion Through Down-Regulation of Prostaglandin E Receptor 2.OncoTargets and therapy · 2020Article
- Histone lysine demethylase KDM4B regulates the alternative splicing of the androgen receptor in response to androgen deprivation.Nucleic acids research · 2019Article
- CREB5 Promotes Resistance to Androgen-Receptor Antagonists and Androgen Deprivation in Prostate Cancer.Cell reports · 2019Article
- G protein-coupled receptor kinase 5 modifies cancer cell resistance to paclitaxel.Molecular and cellular biochemistry · 2019Article
- Neuroendocrine Differentiation of Prostate Cancer-An Intriguing Example of Tumor Evolution at Play.Cancers · 2019Review
- Arginine vasopressin receptor 1a is a therapeutic target for castration-resistant prostate cancer.Science translational medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 8 institutions in 2 countries.
Funding
Abstract
Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer that commonly arises through neuroendocrine differentiation (NED) of prostate adenocarcinoma (PAC) after therapy, such as radiation therapy and androgen deprivation treatment (ADT). No effective therapeutic is available for NEPC and its molecular mechanisms remain poorly understood. We have reported that G protein-coupled receptor kinase 3 (GRK3, also called ADRBK2) promotes prostate cancer progression. In this study, we demonstrate that the ADT-activated cAMP response element binding protein (CREB) directly targets and induces GRK3. We show GRK3 expression is higher in NEPC than in PAC cells and mouse models, and it positively correlates with the expression and activity of CREB in human prostate cancers. Notably, overexpression of GRK3 in PAC cells increased the expression of NE markers in a kinase activity dependent manner. Conversely, silencing GRK3 blocked CREB-induced NED in PAC cells, reversed NE phenotypes and inhibited proliferation of NEPC cells. Taken together, these results indicate that GRK3 is a new critical activator of NE phenotypes and mediator of CREB activation in promoting NED of prostate cancer cells.
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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.