ArticleOncotarget2015
MED1 mediates androgen receptor splice variant induced gene expression in the absence of ligand.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 34 citations in OpenAlex.
- The MicroRNA miR-454 and the mediator complex component MED12 are regulators of the androgen receptor pathway in prostate cancer.Scientific reports · 2025Article
- Review
- Dynamic phase separation of the androgen receptor and its coactivators key to regulate gene expression.Nucleic acids research · 2023Article
- A compendium of Androgen Receptor Variant 7 target genes and their role in Castration Resistant Prostate Cancer.Frontiers in oncology · 2023Review
- Mediator subunit MED1 differentially modulates mutant thyroid hormone receptor intracellular dynamics in Resistance to Thyroid Hormone syndrome.Molecular and cellular endocrinology · 2023Article
- Phosphorylated MED1 links transcription recycling and cancer growth.Nucleic acids research · 2022Article
- Chromatin and Epigenetic Dysregulation of Prostate Cancer Development, Progression, and Therapeutic Response.Cancers · 2021Review
- DNA methylation in promoter regions of genes involved in the reproductive and metabolic function of children born to women with PCOS.Epigenetics · 2020Article
- The potential role of circRNA_004229 in hair/epidermal regulation after MED1 ablation in keratinocytes.RSC advances · 2019Article
- Role of Alternative Splicing in Prostate Cancer Aggressiveness and Drug Resistance in African Americans.Advances in experimental medicine and biology · 2019Review
- Current strategies for targeting the activity of androgen receptor variants.Asian journal of urology · 2019Review
- Down-regulation of AR splice variants through XPO1 suppression contributes to the inhibition of prostate cancer progression.Oncotarget · 2018Article
- Review
- Article
- DBC1 promotes castration-resistant prostate cancer by positively regulating DNA binding and stability of AR-V7.Oncogene · 2018Article
- Driver pattern identification over the gene co-expression of drug response in ovarian cancer by integrating high throughput genomics data.Scientific reports · 2017Article
- Clinical relevance of androgen receptor alterations in prostate cancer.Endocrine connections · 2017Review
- Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation.Cancer research · 2017Article
- RNA splicing and splicing regulator changes in prostate cancer pathology.Human genetics · 2017Review
- Bromodomain protein 4 discriminates tissue-specific super-enhancers containing disease-specific susceptibility loci in prostate and breast cancer.BMC genomics · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The appearance of constitutively active androgen receptor splice variants (AR-Vs) has been proposed as one of the causes of castration-resistant prostate cancer (CRPC). However, the underlying mechanism of AR-Vs in CRPC transcriptional regulation has not been defined. A distinct transcriptome enriched with cell cycle genes, e.g. UBE2C, has been associated with AR-Vs, which indicates the possibility of an altered transcriptional mechanism when compared to full-length wild-type AR (ARfl). Importantly, a recent study reported the critical role of p-MED1 in enhancing UBE2C expression through a locus looping pattern, which only occurs in CRPC but not in androgen-dependent prostate cancer (ADPC). To investigate the potential correlation between AR-V and MED1, in the present study we performed protein co-immunoprecipitation, chromatin immunoprecipitation, and cell proliferation assays and found that MED1 is necessary for ARv567es induced UBE2C up-regulation and subsequent prostate cancer cell growth. Furthermore, p-MED1 is bound to ARv567es independent of full-length AR; p-MED1 has higher recruitment to UBE2C promoter and enhancer regions in the presence of ARv567es. Our data indicate that p-MED1 serves as a key mediator in ARv567es induced gene expression and suggests a mechanism by which AR-Vs promote the development and progression of CRPC.
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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.