ArticleOncotarget2017
Therapy-induced developmental reprogramming of prostate cancer cells and acquired therapy resistance.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Therapy as a State-Generator: Dynamic Phenotypic Landscapes and Adaptive Stress Circuits in Chemotherapy Resistance of Breast Cancer.Antioxidants (Basel, Switzerland) · 2026Review
- PROCA11 early activation fuels prostate cancer neuroendocrine traits by regulating cell survival and migration.iScience · 2025Article
- Actin dysregulation induces neuroendocrine plasticity and immune evasion: a vulnerability of small cell lung cancer.Nature communications · 2025Article
- ONECUT2 acts as a lineage plasticity driver in adenocarcinoma as well as neuroendocrine variants of prostate cancer.Nucleic acids research · 2024Article
- Targeting valine catabolism to inhibit metabolic reprogramming in prostate cancer.Cell death & disease · 2024Article
- ONECUT2 Activates Diverse Resistance Drivers of Androgen Receptor-Independent Heterogeneity in Prostate Cancer.bioRxiv : the preprint server for biology · 2023Article
- Genomic Evolution and Transcriptional Changes in the Evolution of Prostate Cancer into Neuroendocrine and Ductal Carcinoma Types.International journal of molecular sciences · 2023Article
- A Pitfall of the Androgen Deprivation Therapy for Salivary Duct Carcinoma: Hormonal Therapy-Induced Castrate-Resistant Prostate Cancer.Journal of maxillofacial and oral surgery · 2022Article
- Extensive androgen receptor enhancer heterogeneity in primary prostate cancers underlies transcriptional diversity and metastatic potential.Nature communications · 2022Article
- Changes in prostate-specific antigen kinetics during androgen-deprivation therapy as a predictor of response to abiraterone in chemonaïve patients with metastatic castration-resistant prostate cancer.Investigative and clinical urology · 2022Article
- Advances in neuroendocrine prostate cancer research: From model construction to molecular network analyses.Laboratory investigation; a journal of technical methods and pathology · 2022Review
- Wntless expression promotes lineage plasticity and is associated with neuroendocrine prostate cancer.American journal of clinical and experimental urology · 2022Article
- The Androgen Receptor and Its Crosstalk With the Src Kinase During Castrate-Resistant Prostate Cancer Progression.Frontiers in oncology · 2022Review
- Prostate Cancer Epigenetic Plasticity and Enhancer Heterogeneity: Molecular Causes, Consequences and Clinical Implications.Advances in experimental medicine and biology · 2022Review
- The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer.Nature communications · 2021Article
- Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs.Non-coding RNA · 2021Review
- Radical cystoprostatectomy with orthotopic neobladder for a case of treatment emergent neuroendocrine prostate cancer presenting as bladder mass with hematuria-a rare instance of tumor remission after local control.Asian journal of urology · 2021Article
- Decoding the heterogeneous landscape in the development prostate cancer.Oncology letters · 2021Review
- Review
- Glioma Stem Cells as Immunotherapeutic Targets: Advancements and Challenges.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
27 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment-induced neuroendocrine transdifferentiation (NEtD) complicates therapies for metastatic prostate cancer (PCa). Based on evidence that PCa cells can transdifferentiate to other neuroectodermally-derived cell lineages in vitro, we proposed that NEtD requires first an intermediary reprogramming to metastable cancer stem-like cells (CSCs) of a neural class and we demonstrate that several different AR+/PSA+ PCa cell lines were efficiently reprogrammed to, maintained and propagated as CSCs by growth in androgen-free neural/neural crest (N/NC) stem medium. Such reprogrammed cells lost features of prostate differentiation; gained features of N/NC stem cells and tumor-initiating potential; were resistant to androgen signaling inhibition; and acquired an invasive phenotype in vitro and in vivo. When placed back into serum-containing mediums, reprogrammed cells could be re-differentiated to N-/NC-derived cell lineages or return back to an AR+ prostate-like state. Once returned, the AR+ cells were resistant to androgen signaling inhibition. Acute androgen deprivation or anti-androgen treatment in serum-containing medium led to the transient appearance of a sub-population of cells with similar characteristics. Finally, a 132 gene signature derived from reprogrammed PCa cell lines distinguished tumors from PCa patients with adverse outcomes. This model may explain neural manifestations of PCa associated with lethal disease. The metastable nature of the reprogrammed stem-like PCa cells suggests that cycles of PCa cell reprogramming followed by re-differentiation may support disease progression and therapeutic resistance. The ability of a gene signature from reprogrammed PCa cells to identify tumors from patients with metastasis or PCa-specific mortality implies that developmental reprogramming is linked to aggressive tumor behaviors.
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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.