ArticleScience (New York, N.Y.)2017
SOX2 promotes lineage plasticity and antiandrogen resistance in TP53- and RB1-deficient prostate cancer.
Article in Science (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 746 papers.
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Who cites it
746 citing papers in PubMed, 1,023 citations in OpenAlex.
- Article
- Novel approaches to target prostate cancer stem cells driving therapy resistance and cancer progression.Molecular biology reports · 2026Review
- Lineage plasticity-driven immunometabolic state transitions in advanced prostate cancer: biomarkers and therapeutic stratification.Seminars in immunopathology · 2026Review
- Dysregulation of neuronal androgen receptor signaling by divergent collaborative transcription factors in Alzheimer's disease.iScience · 2026Article
- Non-conventional histologies of prostate cancer: from morphology to biology-driven precision oncology.The oncologist · 2026Review
- Article
- ERG Orchestrates a Dedifferentiation-Senescence-Inflammation Triad in Prostate Cancer.Molecular cancer research : MCR · 2026Article
- Spatial and Epigenetic Polarity of the AR Promoter During Prostate Cancer Progression: An In Silico Analysis.International journal of molecular sciences · 2026Article
- Article
- Reframing cancer therapy through tumor plasticity.Nature cancer · 2026Review
- IRE1 activity is prognostic in localised and metastatic prostate cancer and affects epithelial lineage states.EMBO molecular medicine · 2026Article
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
- Single-cell and spatial RNA sequencing in prostate cancer.Nature reviews. Urology · 2026Review
- Combined BET bromodomain and DNA methyltransferase inhibition targets critical survival pathways in transdifferentiated prostate cancer.JCI insight · 2026Article
- ATP-dependent chromatin remodelers in prostate cancer progression and therapeutic resistance.Endocrinology · 2026Review
- TMEM59L promotes neuroendocrine differentiation and enzalutamide resistance in prostate cancer by regulating MUC1/β-catenin/MYC axis.Clinical and translational medicine · 2026Article
- WSB1-Mediated PSMA Ubiquitination Promotes Enzalutamide-Induced Neuroendocrine-like Transition in Patient-Derived Prostate Cancer Spheroids.International journal of molecular sciences · 2026Article
- Systematic analysis of hippo pathway signaling identifies TEAD1 as a transcriptional regulator of neuroendocrine prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- The Great Escape: the systems biology of endocrine resistance and lineage plasticity.Endocrine-related cancer · 2026Review
- Canonical Wnt signaling in the regulation of prostate cancer stem cells: a key driver of castration-resistant prostate cancer and a therapeutic opportunity.Journal of translational medicine · 2026Review
686 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 3 institutions in 2 countries.
Funding
Abstract
Some cancers evade targeted therapies through a mechanism known as lineage plasticity, whereby tumor cells acquire phenotypic characteristics of a cell lineage whose survival no longer depends on the drug target. We use in vitro and in vivo human prostate cancer models to show that these tumors can develop resistance to the antiandrogen drug enzalutamide by a phenotypic shift from androgen receptor (AR)-dependent luminal epithelial cells to AR-independent basal-like cells. This lineage plasticity is enabled by the loss of TP53 and RB1 function, is mediated by increased expression of the reprogramming transcription factor SOX2, and can be reversed by restoring TP53 and RB1 function or by inhibiting SOX2 expression. Thus, mutations in tumor suppressor genes can create a state of increased cellular plasticity that, when challenged with antiandrogen therapy, promotes resistance through lineage switching.
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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.