ArticleOncotarget2016
REST reduction is essential for hypoxia-induced neuroendocrine differentiation of prostate cancer cells by activating autophagy signaling.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Article
- Article
- OPRK1 drives SLC9A3R1 progression to neuroendocrine prostate cancer.Cell death & disease · 2025Article
- High cereblon expression in neuroendocrine cancer confers vulnerability to GSPT1 molecular glue degrader.Experimental hematology & oncology · 2025Article
- ETV5 reduces androgen receptor expression and induces neural stem-like properties during neuroendocrine prostate cancer development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The molecular pathogenesis of SOX2 in prostate cancer.Discover oncology · 2025Review
- Androgen deprivation induces neuroendocrine phenotypes in prostate cancer cells through CREB1/EZH2-mediated downregulation of REST.Cell death discovery · 2024Article
- Regulation of Molecular Biomarkers Associated with the Progression of Prostate Cancer.International journal of molecular sciences · 2024Review
- The lncRNA TPT1-AS1 promotes the survival of neuroendocrine prostate cancer cells by facilitating autophagy.American journal of cancer research · 2024Article
- Androgen deprivation induces neuroendocrine phenotypes in prostate cancer cells through CREB1/EZH2-mediated downregulation of REST.Research square · 2023Article
- Recent Advances in the Role of Autophagy in Endocrine-Dependent Tumors.Endocrine reviews · 2023Review
- Lineage plasticity and treatment resistance in prostate cancer: the intersection of genetics, epigenetics, and evolution.Frontiers in endocrinology · 2023Review
- REST-repressed lncRNA LINC01801 induces neuroendocrine differentiation in prostate cancer via transcriptional activation of autophagy.American journal of cancer research · 2023Article
- AMPK's double-faced role in advanced stages of prostate cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Advances in neuroendocrine prostate cancer research: From model construction to molecular network analyses.Laboratory investigation; a journal of technical methods and pathology · 2022Review
- Role of MicroRNAs in Neuroendocrine Prostate Cancer.Non-coding RNA · 2022Review
- Targeting Protein Arginine Methyltransferase 5 Suppresses Radiation-induced Neuroendocrine Differentiation and Sensitizes Prostate Cancer Cells to Radiation.Molecular cancer therapeutics · 2022Article
- RB1 loss in castration-resistant prostate cancer confers vulnerability to LSD1 inhibition.Oncogene · 2022Article
- The central role of Sphingosine kinase 1 in the development of neuroendocrine prostate cancer (NEPC): A new targeted therapy of NEPC.Clinical and translational medicine · 2022Article
- The Role of Epigenetic Change in Therapy-Induced Neuroendocrine Prostate Cancer Lineage Plasticity.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) with neuroendocrine differentiation (NED) is tightly associated with hormone refractory PCa (HRPC), an aggressive form of cancer that is nearly impossible to treat. Determining the mechanism of the development of NED may yield novel therapeutic strategies for HRPC. Here, we first demonstrate that repressor element-1 silencing transcription factor (REST), a transcriptional repressor of neuronal genes that has been implicated in androgen-deprivation and IL-6 induced NED, is essential for hypoxia-induced NED of PCa cells. Bioinformatics analysis of transcriptome profiles of REST knockdown during hypoxia treatment demonstrated that REST is a master regulator of hypoxia-induced genes. Gene set enrichment analysis (GSEA) of hypoxia and REST knockdown co-upregulated genes revealed their correlation with HRPC. Consistently, gene ontology (GO) analysis showed that REST reduction potential associated with hypoxia-induced tumorigenesis, NE development, and AMPK pathway activation. Emerging reports have revealed that AMPK activation is a potential mechanism for hypoxia-induced autophagy. In line with this, we demonstrate that REST knockdown alone is capable of activating AMPK and autophagy activation is essential for hypoxia-induced NED of PCa cells. Here, making using of in vitro cell-based assay for NED, we reveal a new role for the transcriptional repressor REST in hypoxia-induced NED and characterized a sequential molecular mechanism downstream of REST resulting in AMPK phosphorylation and autophagy activation, which may be a common signaling pathway leading to NED of PCa.
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