Suscripción a Biblioteca: Guest
Portal Digitalde Biblioteca Digital eLibros Revistas Referencias y Libros de Ponencias Colecciones
Critical Reviews™ in Eukaryotic Gene Expression
Factor de Impacto: 1.841 Factor de Impacto de 5 años: 1.927 SJR: 0.627 SNIP: 0.516 CiteScore™: 1.96

ISSN Imprimir: 1045-4403
ISSN En Línea: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.v14.i4.40
14 pages

Neuroendocrine Cells in Prostate Cancer

George P. Amorino
Department of Microbiology, University of Virginia Health Sciences Center, Charlottesville, VA 22908
Sarah J. Parsons
Department of Microbiology, University of Virginia Health Sciences Center, Charlottesville, VA 22908

SINOPSIS

Neuroendocrine (NE) cells are found in prostate tumors, and their incidence is considered a promising prognostic indicator for the development of androgen-independent disease. NE cells are derived from non-NE prostate cancer cells and secrete factors that can act in a paracrine manner to stimulate the survival, growth, motility, and metastatic potential of prostatic carcinoma cells. Factors such as IL-6, epinephrine, and forskolin induce NE differentiation in prostate cancer cells; the mechanisms involve increases in intracellular cAMP, protein kinase A (PKA) activation and reduced intracellular calcium levels. Transcription factors implicated in the acquisition of NE characteristics by prostate cancer cells include STAT3, CREB, EGR1, c-fos, and NF-κB. Expression of Chromogranin A, neuron-specific enolase, bcl-2, and the androgen receptor are modulated during NE differentiation and serve as molecular markers for NE cells. Most importantly, NE cells secrete neuropeptides, such as bombesin, neurotensin, PTHrP, serotonin, and calcitonin, which trigger growth and survival responses in androgen-independent prostate cancer cells. Prostate cancer cell receptors that play a role in these processes include the gastrin-releasing peptide (GRP) receptor, neurotensin receptors, and the epidermal growth-factor receptor (EGFR). Signal-transduction molecules activated by these neuropeptides include Src, focal adhesion kinase (FAK), ERK, and PI3K/Akt, with subsequent activation of Elk-1, NF-κB, and c-myc transcription factors. A multitude of genes are then expressed by prostate cancer cells, which are involved in proliferation, anti-apoptosis, migration, metastasis, and angiogenesis. Targeting of these pathways at multiple levels can be exploited to inhibit the process by which NE cells contribute to the progression of androgen-independent, treatment-refractory prostate cancer.


Articles with similar content:

Oncogene-lnitiated Aberrant Signaling Engenders the Metastatic Phenotype: Synergistic Transcription Factor Interactions are Targets for Cancer Therapy
Critical Reviews™ in Oncogenesis, Vol.7, 1996, issue 3-4
David T. Denhardt
Parathyroid Hormone-Related Protein in Prostate Cancer
Critical Reviews™ in Eukaryotic Gene Expression, Vol.15, 2005, issue 1
Subhash Kukreja, Farrokh Asadi
Aberrant Receptor Signaling and Trafficking as Mechanisms in Oncogenesis
Critical Reviews™ in Oncogenesis, Vol.13, 2007, issue 1
Tor Erik Rusten, Kaisa Haglund, Harald Stenmark
Regulation of FAK Activity by Tetraspan Proteins: Potential Clinical Implications in Cancer
Critical Reviews™ in Oncogenesis, Vol.20, 2015, issue 5-6
Yu Qin, Lynn Gordon, Madhuri Wadehra, Shabnam Mohandessi
Cell Polarity: A Link to Epithelial–Mesenchymal Transition and Vascular Mimicry
Critical Reviews™ in Eukaryotic Gene Expression, Vol.28, 2018, issue 2
Susinjan Bhattacharya