Reduction of ventral prostate weight by finasteride is associated with suppression of insulin-like growth factor I (IGF-I) and IGF-I receptor genes and with an increase in IGF binding protein 3.

Paper

Reduction of ventral prostate weight by finasteride is associated with suppression of insulin-like growth factor I (IGF-I) and IGF-I receptor genes and with an increase in IGF binding protein 3.

Published Jan 15, 1998 · H. Huynh, R. Seyam, G. Brock

Cancer research

Q1 SJR score

53

Citations

1

Influential Citations

Semantic Scholar

Abstract

Finasteride, a competitive and specific inhibitor of 5alpha-reductase, is widely used in the treatment of symptomatic benign prostatic hyperplasia. We demonstrate here that finasteride, when administered in an in vivo experimental system, caused ventral prostate regression. Intraprostatic dihydrotestosterone levels decreased, whereas testosterone levels increased in a dose-dependent manner following finasteride treatment. Finasteride also inhibited the expression of insulin-like growth factor (IGF)-I and IGF-I receptor genes in the ventral prostate. Finasteride significantly increased IGF binding protein-3 and slightly decreased IGF binding protein-2, -4, and -5 gene expression. Because IGFs are potent mitogens for prostate epithelial cells, this newly described activity of finasteride may contribute to its antiproliferative properties, particularly with regard to the inhibition of prostate growth seen clinically and in animal models.

Non-RCT

Animal Study

Study Snapshot

Finasteride causes ventral prostate regression and increases testosterone levels, potentially contributing to its antiproliferative properties in treating benign prostatic hyperplasia.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Reduction of ventral prostate weight by finasteride is associated with suppression of insulin-like growth factor I (IGF-I) and IGF-I receptor genes and with an increase in IGF binding protein 3.

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References

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Castration-induced apoptosis in the rat ventral prostate is associated with increased expression of IGFBP-2,-3,-4, and -5, which may play a role in prostate cancer cell death.

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IGFBP-3 induces apoptosis through a novel pathway independent of p53 and IGFIGF receptor-mediated cell survival, mediating TGF-1-induced apoptosis in PC-3 cells.

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Mac25 is a new member of the IGFBP family, IGFBP-7, which specifically binds IGFs and may function as a growth-suppressing factor in normal tissue and cancer cells.

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The antiestrogen ICI 182780 inhibits breast cancer cell growth by increasing IGFBP-5, suggesting a role for IGFBP-5 in modulating breast cancer proliferation by estrogens and antiestrogens.

Citations

Finasteride-Induced Inhibition of 5α-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study

Finasteride-induced hormonal imbalance in rats can cause kidney damage, suggesting the need for special monitoring and diagnostics in patients with renal dysfunction.

Allopregnanolone Alters the Gene Expression Profile of Human Glioblastoma Cells

Allopregnanolone and progesterone both regulate different sets of genes involved in glioblastoma growth, suggesting potential therapeutic targets for glioblastoma treatment.

Management of Benign Prostatic Hyperplasia: Could Dietary Polyphenols Be an Alternative to Existing Therapies?

Dietary polyphenols show promise in managing benign prostatic hyperplasia, but may not replace existing therapies.

Antiangiogenic therapy effects on age-associated matrix metalloproteinase-9 (MMP-9) and insulin-like growth factor receptor-1 (IGFR-1) responses: a comparative study of prostate disorders in aged and TRAMP mice

Antiangiogenic therapies can help minimize prostate imbalance during senescence by reducing inflammation and neoplastic lesions, with a combination of different agents being more effective.

The influence of growth hormone/insulin-like growth factor deficiency on prostatic dysplasia in pbARR2-Cre, PTEN knockout mice

PTEN loss does not initiate prostate carcinogenesis, but may impact the progression of dysplastic prostatic cells once transformed.