Prostate Development and Carcinogenesis

Wong, Yi‐Lee; Wang, X.H.; Ling, Ming-Tat

doi:10.1016/s0074-7696(03)01008-8

Cited by 25 publications

(17 citation statements)

References 254 publications

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“…These results suggested that the site of IGF-I may vary at different stage after castration; other studies also proved that the IGF-I synthesis may be different in certain circumstance and vary in different species. [15][16][17] In conclusion, we report here that although IGF-I of local VP decreases sharply in short-stage castration, its levels increase gradually and remain at high levels at least until 24 weeks after castration. IGF-I may act as a replacement for androgen by autocrine methods in the case of long-term castration.…”

Section: Igf-i Of Vp F Gao Et Alsupporting

confidence: 50%

“…3,14 IGF-I, one of the epithelial-stromal interaction factors, promotes prostate epithelial proliferation and anti-apoptosis through paracrine or autocrine way and is principally synthesized in prostate stroma or in the epithelium, or in both of these tissue compartments. [15][16][17] Previous study reported that IGF-I is synthesized mainly by stroma in short-stage castration, and may have a role through paracrine or autocrine way; 11 however, the sites of IGF-1 production in long-term castration (up to 24 weeks) is still unknown.…”

Section: Introductionmentioning

confidence: 99%

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Local insulin-like growth factor-I of ventral prostate was upregulated during long-term castration and may function through the autocrine system

Gao

Yang

Luo

et al. 2011

Prostate Cancer Prostatic Dis

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The insulin-like growth factor I (IGF-I) is one of the main mitogens and anti-apoptotic factors, which has an important role in cell proliferation, inhibiting cell death in prostate cancer (PCa), and may act as a replacement for androgen after castration. Characterizing the changes in local IGF-I levels in the prostate after castration, is therefore of great importance for doctors to guide and select therapy models after surgical castration in men with PCa. The present study was performed to detect IGF-I of local ventral prostate (VP) at intervals up to 24 weeks after castration by a combination of reverse transcriptase PCR, western-blot, immunohistochemistry and immunofluorescence. We found IGF-I to be decreased sharply after castration and that mRNA and protein levels reached their minimum at 2 days and 5 days, respectively. The level of IGF-I increased gradually and although mRNA levels remained high for longer than 2 weeks, protein levels remained high for longer than 4 weeks. The epithelium cells of VP express IGF-I and its receptor longer than 2 weeks after castration. These findings suggested that although IGF-I of local VP decreases sharply in short-stage castration, its levels increase gradually and remain at high levels at least until 24 weeks. IGF-I synthesized mainly from epithelial cells, which may function through the autocrine system longer than 2 weeks castration.

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Section: Igf-i Of Vp F Gao Et Alsupporting

confidence: 50%

Section: Introductionmentioning

confidence: 99%

Local insulin-like growth factor-I of ventral prostate was upregulated during long-term castration and may function through the autocrine system

Gao

Yang

Luo

et al. 2011

Prostate Cancer Prostatic Dis

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“…Similarly, mice lacking only a single allele of p44 develop prostatic hyperplasia. Prostate tumorigenesis is a multistep process involving both genetic alterations (activation of oncogenes and inactivation of tumor suppressor genes) of the ECs and perturbation of stromal-epithelial interactions (Wong et al 2003). The p44 translocation is a very early event leading to the proliferation of prostatic ECs (dividing one layer into two and more layers).…”

Section: The Role Of P44 In Prostate Tumorigenesismentioning

confidence: 99%

Roles of the androgen receptor cofactor p44 in the growth of prostate epithelial cells

Zhou¹,

Wu²,

Lee³

et al. 2006

Journal of Molecular Endocrinology

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Various cofactors have been shown to regulate androgen receptor (AR) transactivation, but their physiological functions in the AR pathway and prostate tumorigenesis are undefined. Here, we found that AR cofactor (p44) translocation from the nucleus to the cytoplasm in prostate epithelial cells (ECs) is associated with prostate tumorigenesis. The forced nuclear localization of p44 inhibited prostate cancer cell growth by G1 cell-cycle arrest. Consistently, mice lacking one allele of the p44 gene developed prostatic hyperplasia. Therefore, p44 is required for proper expression of AR-target genes to maintain the differentiation of prostate ECs, and p44 translocation from the nucleus into the cytoplasm in prostate cancer cells or loss of one allele in mouse results in excessive prostate EC proliferation.

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“…In normal tissue, these interactions are often paracrine, with receptors for a particular GF present on epithelial cells and production of the GF by stromal cells. In cancer, some GF pathways become autocrine, thus enabling epithelial cells, which express a GF and its receptor, to grow independently of stromal cells [79][80][81].…”

Section: Introductionmentioning

confidence: 99%