ArticleThe Journal of biological chemistry2013
The ETS domain transcription factor ELK1 directs a critical component of growth signaling by the androgen receptor in prostate cancer cells.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- Shikonin promotes osteogenic differentiation of periodontal ligament stem cells by modulating the p38 MAPK/ETS transcription factor 1/cementum protein 1 axis in vitro.Journal of cell communication and signaling · 2026Article
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- The Small Molecule Antagonist KCI807 Disrupts Association of the Amino-Terminal Domain of the Androgen Receptor with ELK1 by Modulating the Adjacent DNA Binding Domain.Molecular pharmacology · 2023Article
- Glucose Homeostasis and Pancreatic Islet Size Are Regulated by the Transcription Factors Elk-1 and Egr-1 and the Protein Phosphatase Calcineurin.International journal of molecular sciences · 2023Review
- Role of ELK1 in regulating colorectal cancer progression: miR-31-5p/CDIP1 axis in CRC pathogenesis.PeerJ · 2023Article
- Identification of ELK1 interacting peptide segments in the androgen receptor.The Biochemical journal · 2022Article
- ELK1-mediated YTHDF1 drives prostate cancer progression by facilitating the translation of Polo-like kinase 1 in an m6A dependent manner.International journal of biological sciences · 2022Article
- Article
- Pairwise Heuristic Sequence Alignment Algorithm Based on Deep Reinforcement Learning.IEEE open journal of engineering in medicine and biology · 2021Article
- MED19 alters AR occupancy and gene expression in prostate cancer cells, driving MAOA expression and growth under low androgen.PLoS genetics · 2021Article
- Clinical association of progesterone receptor isoform A with breast cancer metastasis consistent with its unique mechanistic role in preclinical models.BMC cancer · 2020Article
- CITED2 and the modulation of the hypoxic response in cancer.World journal of clinical oncology · 2020Review
- Ras and Wnt Interaction Contribute in Prostate Cancer Bone Metastasis.Molecules (Basel, Switzerland) · 2020Review
- The ternary complex factor protein ELK1 is an independent prognosticator of disease recurrence in prostate cancer.The Prostate · 2020Article
- Strategy for Tumor-Selective Disruption of Androgen Receptor Function in the Spectrum of Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Aberrant expression of CITED2 promotes prostate cancer metastasis by activating the nucleolin-AKT pathway.Nature communications · 2018Article
- AIRE promotes androgen-independent prostate cancer by directly regulating IL-6 and modulating tumor microenvironment.Oncogenesis · 2018Article
- Divergence in DNA Specificity among Paralogous Transcription Factors Contributes to Their Differential In Vivo Binding.Cell systems · 2018Article
- Expression of Phospho-ELK1 and Its Prognostic Significance in Urothelial Carcinoma of the Upper Urinary Tract.International journal of molecular sciences · 2018Article
- Histone deacetylase 6 (HDAC6) deacetylates extracellular signal-regulated kinase 1 (ERK1) and thereby stimulates ERK1 activity.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The androgen receptor (AR) is essential for diverse aspects of prostate development and function. Molecular mechanisms by which prostate cancer (PC) cells redirect AR signaling to genes that primarily support growth are unclear. A systematic search for critical AR-tethering proteins led to ELK1, an ETS transcription factor of the ternary complex factor subfamily. Although genetically redundant, ELK1 was obligatory for AR-dependent growth and clonogenic survival in both hormone-dependent PC and castration-recurrent PC cells but not for AR-negative cell growth. AR required ELK1 to up-regulate a major subset of its target genes that was strongly and primarily enriched for cell growth functions. AR functioned as a coactivator of ELK1 by association through its A/B domain, bypassing the classical mechanism of ELK1 activation by phosphorylation and without inducing ternary complex target genes. The ELK1-AR synergy per se was ligand-independent, although it required ligand for nuclear localization of AR as targeting the AR A/B domain to the nucleus recapitulated the action of hormone; accordingly, Casodex was a poor antagonist of the synergy. ELK3, the closest substitute for ELK1 in structure/function and genome recognition, did not interact with AR. ELK1 thus directs selective and sustained gene induction that is a substantial and critical component of growth signaling by AR in PC cells. The ELK1-AR interaction offers a functionally tumor-selective drug target.
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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.