ArticleBritish journal of cancer2022
MYB interacts with androgen receptor, sustains its ligand-independent activation and promotes castration resistance in prostate cancer.
Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Genomic landscape and precision therapy in prostate cancer: current status and future directions.NPJ precision oncology · 2026Review
- Emerging role of HIC1 in prostate cancer progression and therapeutic response: A novel perspective.Journal of cell communication and signaling · 2025Article
- MYB and HIF1α crosstalk drives hypoxia-induced transcriptional reprogramming and adaptive signaling alterations in pancreatic cancer.Cancer letters · 2025Article
- MYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance.Journal of ovarian research · 2025Article
- Comparative Analysis of MYB Expression by Immunohistochemistry and RNA Sequencing in Clinical Gene Fusion Detection in Adenoid Cystic Carcinoma.Head and neck pathology · 2024Article
- Proto-oncogene c-Myb potentiates cisplatin resistance of ovarian cancer cells by downregulating lncRNA NKILA and modulating cancer stemness and LIN28A-let7 axis.Journal of ovarian research · 2024Article
- Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024Review
- From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies.Cancer metastasis reviews · 2024Review
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Article
- MYB sustains hypoxic survival of pancreatic cancer cells by facilitating metabolic reprogramming.EMBO reports · 2023Article
- Post-prostatic-massage urine exosomes of men with chronic prostatitis/chronic pelvic pain syndrome carry prostate-cancer-typical microRNAs and activate proto-oncogenes.Molecular oncology · 2023Article
- Mitochondrial Alterations in Prostate Cancer: Roles in Pathobiology and Racial Disparities.International journal of molecular sciences · 2023Review
- The androgen receptor-targeted proteolysis targeting chimera and other alternative therapeutic choices in overcoming the resistance to androgen deprivation treatment in prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Editorial: Molecular drivers of prostate cancer pathogenesis and therapy resistance.Frontiers in cell and developmental biology · 2023Article
- Review
- Second generation androgen receptor antagonists and challenges in prostate cancer treatment.Cell death & disease · 2022Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundAberrant activation of androgen receptor signalling following castration therapy is a common clinical observation in prostate cancer (PCa). Earlier, we demonstrated the role of MYB overexpression in androgen-depletion resistance and PCa aggressiveness. Here, we investigated MYB-androgen receptor (AR) crosstalk and its functional significance.
methodsInteraction and co-localization of MYB and AR were examined by co-immunoprecipitation and immunofluorescence analyses, respectively. Protein levels were measured by immunoblot analysis and enzyme-linked immunosorbent assay. The role of MYB in ligand-independent AR transcriptional activity and combinatorial gene regulation was studied by promoter-reporter and chromatin immunoprecipitation assays. The functional significance of MYB in castration resistance was determined using an orthotopic mouse model.
resultsMYB and AR interact and co-localize in the PCa cells. MYB-overexpressing PCa cells retain AR in the nucleus even when cultured under androgen-deprived conditions. AR transcriptional activity is also sustained in MYB-overexpressing cells in the absence of androgens. MYB binds and promotes AR occupancy to the KLK3 promoter. MYB-overexpressing PCa cells exhibit greater tumorigenicity when implanted orthotopically and quickly regain growth following castration leading to shorter mice survival, compared to those carrying low-MYB-expressing prostate tumours.
conclusionsOur findings reveal a novel MYB-AR crosstalk in PCa and establish its role in castration resistance.
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