ArticleOncotarget2014
CAMK2N1 inhibits prostate cancer progression through androgen receptor-dependent signaling.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 66 citations in OpenAlex.
- CaMKII nucleates an osmotic protein supercomplex to induce cellular bleb expansion.The EMBO journal · 2026Article
- MicroRNA mediated signaling and metabolic reprogramming in oral squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- ANO1: central role and clinical significance in non-neoplastic and neoplastic diseases.Frontiers in immunology · 2025Review
- Updates on Overcoming Bicalutamide Resistance: A Glimpse into Resistance to a Novel Antiandrogen.ACS pharmacology & translational science · 2024Review
- Advances in synthetic lethality modalities for glioblastoma multiforme.Open medicine (Warsaw, Poland) · 2024Review
- Article
- Oncofetal protein glypican-3 is a biomarker and critical regulator of function for neuroendocrine cells in prostate cancer.The Journal of pathology · 2023Article
- Article
- Downregulation of CAMK2N1 due to DNA Hypermethylation Mediated by DNMT1 that Promotes the Progression of Prostate Cancer.Journal of oncology · 2023Article
- The circSPON2/miR-331-3p axis regulates PRMT5, an epigenetic regulator of CAMK2N1 transcription and prostate cancer progression.Molecular cancer · 2022Article
- Review
- Discovery of a New CaMKII-Targeted Synthetic Lethal Therapy against Glioblastoma Stem-like Cells.Cancers · 2022Article
- NcRNA-mediated upregulation of CAMK2N1 is associated with poor prognosis and tumor immune infiltration of gastric cancer.Frontiers in genetics · 2022Article
- CaMKII Mediates TGFβ1-Induced Fibroblasts Activation and Its Cross Talk with Colon Cancer Cells.Digestive diseases and sciences · 2022Article
- A long noncoding RNA-microRNA expression signature predicts metastatic signature in pheochromocytomas and paragangliomas.Endocrine · 2022Article
- The Calcium/Calmodulin-Dependent Kinases II and IV as Therapeutic Targets in Neurodegenerative and Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- Advances in the Regulation of Mammalian Follicle-Stimulating Hormone Secretion.Animals : an open access journal from MDPI · 2021Review
- Prenatal androgen exposure causes a sexually dimorphic transgenerational increase in offspring susceptibility to anxiety disorders.Translational psychiatry · 2021Article
- Does miRNA Expression in the Spent Media Change During Early Embryo Development?Frontiers in veterinary science · 2021Article
- Multi-omics profiling highlights lipid metabolism alterations in pigs fed low-dose antibiotics.BMC genetics · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Castration resistance is a major obstacle to hormonal therapy for prostate cancer patients. Although androgen independence of prostate cancer growth is a known contributing factor to endocrine resistance, the mechanism of androgen receptor deregulation in endocrine resistance is still poorly understood. Herein, the CAMK2N1 was shown to contribute to the human prostate cancer cell growth and survival through AR-dependent signaling. Reduced expression of CAMK2N1 was correlated to recurrence-free survival of prostate cancer patients with high levels of AR expression in their tumor. CAMK2N1 and AR signaling form an auto-regulatory negative feedback loop: CAMK2N1 expression was down-regulated by AR activation; while CAMK2N1 inhibited AR expression and transactivation through CAMKII and AKT pathways. Knockdown of CAMK2N1 in prostate cancer cells alleviated Casodex inhibition of cell growth, while re-expression of CAMK2N1 in castration-resistant cells sensitized the cells to Casodex treatment. Taken together, our findings suggest that CAMK2N1 plays a tumor suppressive role and serves as a crucial determinant of the resistance of prostate cancer to endocrine therapies.
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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.