Journal Article

Recent advances on multiple tumorigenic cascades involved in prostatic cancer progression and targeting therapies

Murielle Mimeault and Surinder K. Batra

in Carcinogenesis

Volume 27, issue 1, pages 1-22
Published in print January 2005 | ISSN: 0143-3334
Published online September 2005 | e-ISSN: 1460-2180 | DOI: https://dx.doi.org/10.1093/carcin/bgi229
Recent advances on multiple tumorigenic cascades involved in prostatic cancer progression and targeting therapies

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Recent advances on differently-expressed gene products and their functions during the progression from localized androgen-dependent states into androgen-independent and metastatic forms of prostate cancer are reported. The expression levels of numerous oncogenes and tumor suppressor genes in distinct prostatic cancer epithelial cell lines and tissues relative to normal prostate cells are described. This is carried out to identify the signaling elements that are altered during the initiation, progression and metastatic process of prostate cancer. Additional information on the interactions between certain deregulated signaling pathways such as androgen receptor (AR), estrogen receptors, epidermal growth factor receptor (EGFR), hedgehog and Wnt/β-catenin cascades in controlling the proliferation, survival and invasion of tumor prostate epithelial cells during the disease progression is described. The emphasis is on the critical functions of the AR and EGF–EGFR systems at all stages during prostate carcinogenesis. Of therapeutic interest, new strategies for the diagnosis and treatment of localized and metastatic forms of prostate cancer by targeting multiple tumorigenic signaling elements are also reported.

Keywords: AR, androgen receptor; CTCs, circulating tumor cells; E2, 17β-estradiol; EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; ER, estrogen receptor; FGF, fibroblast growth factor; GSK3β, glycogensynthase kinase 3β; HGF, hepatocyte growth factor; HRPC, hormone-refractory prostate cancer; 17HSD, 17β-hydroxysteroid dehydrogenase; IGF, insulin-like growth factor; IL-6, interleukin-6; ILK, integrin-linked kinase; MAPK, mitogen-activated protein kinase; MIC-1, macrophage inhibitor cytokine-1; NE, neuroendocrine; NF-κB, nuclear factor kappa-β; PC, prostate cancer; PI3K, phosphatidylinositol 3′-kinase; PIN, prostatic intraepithelial neoplasia; PKA, protein kinase A; PKCδ, protein kinase C-δ; PNI, prostatic perineural invasion; PSA, prostate specific antigen; PTEN, tensin homologue deleted on chromosome 10; RP, radical prostatectomy, siRNA, small interfering RNA; SHH, sonic hedgehog; TCF, T-cell factor; TGF-α, transforming growth factor-α; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor-α; VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth factor receptor

Journal Article.  20762 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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