ArticleNeoplasia (New York, N.Y.)2007
EGF prevents the neuroendocrine differentiation of LNCaP cells induced by serum deprivation: the modulator role of PI3K/Akt.
Article in Neoplasia (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
- Neuroendocrine differentiation: a risk fellow in colorectal cancer.World journal of surgical oncology · 2023Article
- Claudin-3 Loss of Expression Is a Prognostic Marker in Castration-Resistant Prostate Cancer.International journal of molecular sciences · 2023Article
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- Review
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- EGFR-upregulated LIFR promotes SUCLG2-dependent castration resistance and neuroendocrine differentiation of prostate cancer.Oncogene · 2020Article
- SNHG16 promotes tumorigenesis and cisplatin resistance by regulating miR-338-3p/PLK4 pathway in neuroblastoma cells.Cancer cell international · 2020Article
- Anticancer Effects and Mechanisms of Action of Plumbagin: Review of Research Advances.BioMed research international · 2020Review
- Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis.OncoTargets and therapy · 2020Article
- Casticin inhibits breast cancer cell migration and invasion by down-regulation of PI3K/Akt signaling pathway.Bioscience reports · 2018Article
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- The deregulation of miR-17/CCND1 axis during neuroendocrine transdifferentiation of LNCaP prostate cancer cells.PloS one · 2018Article
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- Induction of Neuroendocrine Differentiation in Prostate Cancer Cells by Dovitinib (TKI-258) and its Therapeutic Implications.Translational oncology · 2017Article
- Alterations of androgen receptor-regulated enhancer RNAs (eRNAs) contribute to enzalutamide resistance in castration-resistant prostate cancer.Oncotarget · 2016Article
- Neuroendocrine differentiation in prostate cancer: a mechanism of radioresistance and treatment failure.Frontiers in oncology · 2015Review
- SRPK1 contributes to malignancy of hepatocellular carcinoma through a possible mechanism involving PI3K/Akt.Molecular and cellular biochemistry · 2013Article
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- Involvement of Src in the Adaptation of Cancer Cells under Microenvironmental Stresses.Journal of signal transduction · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The primary focus of this investigation was to study the relationship between neuroendocrine (NE) differentiation and epidermal growth factor (EGF) because both have been implicated in the progression of prostate cancer. For this purpose, we used gefitinib and trastuzumab, which are inhibitors of EGF receptor (EGFR) and ErbB2, respectively. EGF prevents NE differentiation induced by androgen depletion. This effect is prevented by gefitinib, which blocks the activation of EGFR and ErbB2, stimulation of mitogen-activated protein kinase (MAPK), and cell proliferation induced by EGF. Conversely, trastuzumab does not inhibit the effect of EGF on EGFR phosphorylation, MAPK activity, cell proliferation, and NE differentiation, although it reduces ErbB2 levels specifically, suggesting that ErbB2 is not necessary to inhibit NE differentiation. Prevention of NE differentiation by EGF is mediated by a MAPK-dependent mechanism and requires constitutive Akt activation. The abrogation of the PI3K/Akt pathway changes the role of EGF from inhibitor to inductor of NE differentiation. We show that EGFR tyrosine kinase, MAPK, and PI3K inhibitors inhibit the cell proliferation stimulated by EGF but induce the acquisition of NE phenotype. Altogether, the present data should be borne in mind when designing new clinical schedules for the treatment of prostate cancer, including the use of ErbB receptors and associated signaling pathway inhibitors.
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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.