ArticleCells2020
Androgen Deprivation Induces Reprogramming of Prostate Cancer Cells to Stem-Like Cells.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Novel approaches to target prostate cancer stem cells driving therapy resistance and cancer progression.Molecular biology reports · 2026Review
- PARP Inhibition in Prostate Cancer: Current Status, Resistance Mechanisms, and Clinical Challenges.Cells · 2026Review
- MicroRNA Signatures of Prostate Cancer Spheroids in Microfluidic Culture Under Hormone-Deprivation Conditions.Bioengineering (Basel, Switzerland) · 2026Article
- TRPV1 Downregulation Impairs Prostate Cancer Growth: Functional and Translational Insights from Cellular andInternational journal of biological sciences · 2026Article
- Stemness regulation in prostate cancer: prostate cancer stem cells and targeted therapy.Annals of medicine · 2025Review
- Unlocking the Role of OCT4 in Cancer Lineage Plasticity: A Cross-Cancer Perspective with an Emphasis on Prostate Cancer.Biomedicines · 2025Review
- The Use of Neurons Derived from Pluripotent Stem Cells to Study Nerve-Cancer Cell Interactions.International journal of molecular sciences · 2025Review
- CDHu40: a novel marker gene set of neuroendocrine prostate cancer.Briefings in bioinformatics · 2024Article
- Article
- Treatment-induced stemness and lineage plasticity in driving prostate cancer therapy resistance.Cancer heterogeneity and plasticity · 2024Article
- Resistance to 2-Hydroxy-Flutamide in Prostate Cancer Cells Is Associated with the Downregulation of Phosphatidylcholine Biosynthesis and Epigenetic Modifications.International journal of molecular sciences · 2023Article
- Prostate Cancer Stem Cells: Biology and Treatment Implications.International journal of molecular sciences · 2023Review
- The Molecular Biology of Prostate Cancer Stem Cells: From the Past to the Future.International journal of molecular sciences · 2023Review
- Zinc finger protein‑like 1 is a novel neuroendocrine biomarker for prostate cancer.International journal of oncology · 2023Article
- Androgen Deprivation Freezes Hormone-Sensitive Prostate Cancer Cells in a Reversible, Genetically Unstable Quasi-Apoptotic State, Bursting into Full Apoptosis upon Poly(ADP-ribose) Polymerase Inhibition.International journal of molecular sciences · 2023Article
- State-of-the-art therapeutic strategies for targeting cancer stem cells in prostate cancer.Frontiers in oncology · 2023Review
- Alteration of the HIF-1α/VEGF Signaling Pathway and Disruption of the Cell Cycle by Second Generation Carbosilan Dendrimers.Biomacromolecules · 2022Article
- Prostate cancer cells demonstrate unique metabolism and substrate adaptability acutely after androgen deprivation therapy.The Prostate · 2022Article
- Prostate Cancer Stem Cells: The Role of CD133.Cancers · 2022Review
- Prostate cancer as a dedifferentiated organ: androgen receptor, cancer stem cells, and cancer stemness.Essays in biochemistry · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the past few years, cell plasticity has emerged as a mode of targeted therapy evasion in prostate adenocarcinoma. When exposed to anticancer therapies, tumor cells may switch into a different histological subtype, such as the neuroendocrine phenotype which is associated with treatment failure and a poor prognosis. In this study, we demonstrated that long-term androgen signal depletion of prostate LNCaP cells induced a neuroendocrine phenotype followed by re-differentiation towards a "stem-like" state. LNCaP cells incubated for 30 days in charcoal-stripped medium or with the androgen receptor antagonist 2-hydroxyflutamide developed neuroendocrine morphology and increased the expression of the neuroendocrine markers βIII-tubulin and neuron specific enolase (NSE). When cells were incubated for 90 days in androgen-depleted medium, they grew as floating spheres and had enhanced expression of the stem cell markers CD133, ALDH1A1, and the transporter ABCB1A. Additionally, the pluripotent transcription factors Nanog and Oct4 and the angiogenic factor VEGF were up-regulated while the expression of E-cadherin was inhibited. Cell viability revealed that those cells were resistant to docetaxel and 2-hidroxyflutamide. Mechanistically, androgen depletion induced the decrease in AMP-activated kinase (AMPK) expression and activation and stabilization of the hypoxia-inducible factor HIF-1α. Overexpression of AMPK in the stem-like cells decreased the expression of stem markers as well as that of HIF-1α and VEGF while it restored the levels of E-cadherin and PGC-1α. Most importantly, docetaxel sensitivity was restored in stem-like AMPK-transfected cells. Our model provides a new regulatory mechanism of prostate cancer plasticity through AMPK that is worth exploring.
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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.