ArticleThe Journal of clinical investigation2003
Myc confers androgen-independent prostate cancer cell growth.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 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.
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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
113 citing papers in PubMed, 194 citations in OpenAlex.
- Prostate cancer cells' growth is decreased by novel MYC inhibitors.Investigational new drugs · 2026Article
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer.Oncogene · 2025Article
- Cyclin-dependent kinases as mediators of aberrant transcription in prostate cancer.Translational oncology · 2025Review
- Advances in tumor subclone formation and mechanisms of growth and invasion.Journal of translational medicine · 2025Review
- Landscape and prognostic significance of oncogene drivers in metastatic castration sensitive prostate cancer.Translational cancer research · 2024Article
- CDK12-inactivation-induced MYC signaling causes dependency on the splicing kinase SRPK1.Molecular oncology · 2024Article
- Generating a Murine PTEN Null Cell Line to Discover the Key Role of p110β-PAK1 in Castration-Resistant Prostate Cancer Invasion.Molecular cancer research : MCR · 2023Article
- Androgen receptor and MYC transcriptomes are equilibrated in multilayer regulatory circuitries in prostate cancer.The Prostate · 2023Article
- MYC is a regulator of androgen receptor inhibition-induced metabolic requirements in prostate cancer.Cell reports · 2023Article
- Dissecting transcription of the 8q24-MYC locus in prostate cancer recognizes the equilibration between androgen receptor direct and indirect dual-functions.Journal of translational medicine · 2023Article
- Chromosome 8q arm overexpression is associated with worse prostate cancer prognosis.Urologic oncology · 2023Article
- Retraction Note: CBX7 controls the growth of normal and tumor-derived prostate cells by repressing the Ink4a/Arf locus.Oncogene · 2022Article
- Androgen-Responsive Oncogenic lncRNA RP11-1023L17.1 Enhances c-Myc Protein Stability in Prostate Cancer.International journal of molecular sciences · 2022Article
- Article
- The Integration of Metabolomics with Other Omics: Insights into Understanding Prostate Cancer.Metabolites · 2022Review
- CREB5 reprograms FOXA1 nuclear interactions to promote resistance to androgen receptor-targeting therapies.eLife · 2022Article
- THEM6-mediated reprogramming of lipid metabolism supports treatment resistance in prostate cancer.EMBO molecular medicine · 2022Article
- Receptor-interacting protein kinase 2 (RIPK2) stabilizes c-Myc and is a therapeutic target in prostate cancer metastasis.Nature communications · 2022Article
- Article
53 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is one of the most diagnosed and mortal cancers in western countries. A major clinical problem is the development of androgen-independent prostate cancer (AIPC) during antihormonal treatment. The molecular mechanisms underlying the change from androgen dependence to independence of these tumors are poorly understood and represent a challenge to develop new therapies. Based on genetic data showing amplification of the c-myc gene in AIPC, we studied the ability of c-myc to confer AIPC cell growth. Human androgen-dependent prostate cancer cells overexpressing c-myc grew independently of androgens and presented tumorigenic properties in androgen-depleted conditions. Analysis of signalling pathways by pharmacological inhibitors of the androgen receptor (AR) or by RNA interference directed against AR or c-myc showed that c-myc acted downstream of AR through multiple growth effectors. Thus c-myc is required for androgen-dependent growth and following ectopic expression can induce androgen-independent growth. Moreover, RNA interference directed against c-myc showed that growth of human AIPC cells, AR-positive or -negative, required c-myc expression. Furthermore, we showed that c-myc-overexpressing cells retain a functional p53 pathway and thus respond to etoposide.
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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.