ArticleCarcinogenesis2012
Myb overexpression overrides androgen depletion-induced cell cycle arrest and apoptosis in prostate cancer cells, and confers aggressive malignant traits: potential role in castration resistance.
Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Genomic landscape and precision therapy in prostate cancer: current status and future directions.NPJ precision oncology · 2026Review
- MYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance.Journal of ovarian research · 2025Article
- 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
- Streamlined identification of clinically and functionally relevant genetic regulators of lower-tract urogenital development.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Article
- Review
- MYB interacts with androgen receptor, sustains its ligand-independent activation and promotes castration resistance in prostate cancer.British journal of cancer · 2022Article
- Investigating the Role of Obesity in Prostate Cancer and Identifying Biomarkers for Drug Discovery: Systems Biology and Deep Learning Approaches.Molecules (Basel, Switzerland) · 2022Article
- Prostate Cancer Disparities and Management in Southern Africa: Insights into Practices, Norms and Values.Cancer management and research · 2022Review
- Response prediction biomarkers and drug combinations of PARP inhibitors in prostate cancer.Acta pharmacologica Sinica · 2021Review
- Clinicopathologic significance and race-specific prognostic association of MYB overexpression in ovarian cancer.Scientific reports · 2021Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
- Morphological and functional alterations of the prostate tissue during clinical progression in hormonally-naïve, hormonally-treated and castration-resistant patients with metastatic prostate cancer.Oncology letters · 2020Article
- Immune molecular profiling of a multiresistant primary prostate cancer with a neuroendocrine-like phenotype: a case report.BMC urology · 2020Article
- Cellular and Molecular Progression of Prostate Cancer: Models for Basic and Preclinical Research.Cancers · 2020Review
- Therapies Targeted to Androgen Receptor Signaling Axis in Prostate Cancer: Progress, Challenges, and Hope.Cancers · 2019Review
- MYB promotes the growth and metastasis of salivary adenoid cystic carcinoma.International journal of oncology · 2019Article
- The X-linked tumor suppressor TSPX downregulates cancer-drivers/oncogenes in prostate cancer in a C-terminal acidic domain dependent manner.Oncotarget · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Myb, a cellular progenitor of v-Myb oncogenes, is amplified in prostate cancer and exhibits greater amplification frequency in hormone-refractory disease. Here, we have investigated the functional significance of Myb in prostate cancer. Our studies demonstrate Myb expression in all prostate cancer cell lines (LNCaP, C4-2, PC3 and DU145) examined, whereas it is negligibly expressed in normal/benign prostate epithelial cells (RWPE1 and RWPE2). Notably, Myb is significantly upregulated, both at transcript (>60-fold) and protein (>15-fold) levels, in castration-resistant (C4-2) cells as compared with androgen-dependent (LNCaP) prostate cancer cells of the same genotypic lineage. Using loss and gain of function approaches, we demonstrate that Myb promotes and sustains cell cycle progression and survival under androgen-supplemented and -deprived conditions, respectively, through induction of cyclins (A1, D1 and E1), Bcl-xL and Bcl2 and downregulation of p27 and Bax. Interestingly, Myb overexpression is also associated with enhanced prostate-specific antigen expression. Furthermore, our data show a role of Myb in enhanced motility and invasion and decreased homotypic interactions of prostate cancer cells. Myb overexpression is also associated with actin reorganization leading to the formation of filopodia-like cellular protrusions. Immunoblot analyses demonstrate gain of mesenchymal and loss of epithelial markers and vice versa, in Myb-overexpressing LNCaP and -silenced C4-2 cells, respectively, indicating a role of Myb in epithelial to mesenchymal transition. Altogether, our studies provide first experimental evidence for a functional role of Myb in growth and malignant behavior of prostate cancer cells and suggest a novel mechanism for castration resistance.
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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.