ArticleCancer research2011
CaM kinase kinase beta-mediated activation of the growth regulatory kinase AMPK is required for androgen-dependent migration of prostate cancer cells.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
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Who cites it
86 citing papers in PubMed, 143 citations in OpenAlex.
- CAMKV kinase drives neuroblastoma growth and acts as a novel therapeutic target.The Journal of experimental medicine · 2026Article
- Androgen receptor contributes to radioresistance through DNA repair and autophagy in AR-positive prostate cancer cells.bioRxiv : the preprint server for biology · 2025Article
- Effects of empagliflozin and its combination with docetaxel on LNCaP and DU- 145 prostate cancer cell lines: cytotoxicity and molecular pathway analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The role of calcium signaling in organotropic metastasis of cancer.Acta pharmacologica Sinica · 2025Review
- Cholesterol metabolism regulated by CAMKK2-CREB signaling promotes castration-resistant prostate cancer.Cell reports · 2025Article
- CaMKK2: bridging the gap between Ca2+ signaling and energy-sensing.Essays in biochemistry · 2024Review
- Unlocking ferroptosis in prostate cancer - the road to novel therapies and imaging markers.Nature reviews. Urology · 2024Review
- Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity.Cancer research · 2024Article
- CAMKV Kinase Signaling Is a Novel Therapeutic Avenue with Prognostic Relevance in Neuroblastoma.bioRxiv : the preprint server for biology · 2024Article
- Current Understanding of Androgen Signaling in Prostatitis and its Treatment: A Review.Current medicinal chemistry · 2024Review
- Targeting CaMKK2 Inhibits Actin Cytoskeletal Assembly to Suppress Cancer Metastasis.Cancer research · 2023Article
- Cancer Cell-Extrinsic Roles for the Androgen Receptor in Prostate Cancer.Endocrinology · 2023Review
- The role of CaMKK2 in Golgi-associated vesicle trafficking.Biochemical Society transactions · 2023Review
- Increased CaMKK2 Expression Is an Adaptive Response That Maintains the Fitness of Tumor-Infiltrating Natural Killer Cells.Cancer immunology research · 2023Article
- Neuronal CaMKK2 promotes immunosuppression and checkpoint blockade resistance in glioblastoma.Nature communications · 2022Article
- Molecular Mechanisms Underlying CaInternational journal of molecular sciences · 2022Review
- Systemic Ablation ofCells · 2022Article
- Regulation and role of CAMKK2 in prostate cancer.Nature reviews. Urology · 2022Review
- Review
- The Natural Chemotherapeutic Capsaicin Activates AMPK through LKB1 Kinase and TRPV1 Receptors in Prostate Cancer Cells.Pharmaceutics · 2022Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
While patients with advanced prostate cancer initially respond favorably to androgen ablation therapy, most experience a relapse of the disease within 1-2 years. Although hormone-refractory disease is unresponsive to androgen-deprivation, androgen receptor (AR)-regulated signaling pathways remain active and are necessary for cancer progression. Thus, both AR itself and the processes downstream of the receptor remain viable targets for therapeutic intervention. Microarray analysis of multiple clinical cohorts showed that the serine/threonine kinase Ca2+/calmodulin-dependent protein kinase kinase β (CaMKKβ) is both highly expressed in the prostate and further elevated in prostate cancers. Using cellular models of prostate cancer, we have determined that androgens (a) directly increase the expression of a CaMKKβ splice variant and (b) increase functional CaMKKβ protein levels as determined by the phosphorylation of both CaMKI and AMP-activated protein kinase (AMPK), two of CaMKKβ's primary substrates. Importantly, inhibition of the CaMKKβ-AMPK, but not CaMKI, signaling axis in prostate cancer cells by pharmacological inhibitors or siRNA-mediated knockdown blocks androgen-mediated migration and invasion. Conversely, overexpression of CaMKKβ alone leads to both increased AMPK phosphorylation and cell migration. Given the key roles of CaMKKβ and AMPK in the biology of prostate cancer cells, we propose that these enzymes are potential therapeutic targets in prostate cancer.
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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.