Insulin-like growth factors and their binding proteins in prostate cancer: Cause or consequence?☆

Meinbach, David S.; Lokeshwar, Bal L.

doi:10.1016/j.urolonc.2005.12.004

Cited by 48 publications

(48 citation statements)

References 147 publications

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“…We also observed a significant reduction in the levels of IGF-I and IGFBP-3 in men taking Polyphenon E. Levels of IGF and IGFBP-3 have been studied for a number of years and the results are still controversial about their roles in prostate cancer development or progression (53)(54)(55). A recent study concluded that there was no association between levels of these two proteins and prostate cancer, although interestingly, the authors noted that prediagnostic levels of IGFBP-3 correlated with prostate cancer risk, but only for Black men (56).…”

Section: Discussionmentioning

confidence: 87%

Tea Polyphenols Decrease Serum Levels of Prostate-Specific Antigen, Hepatocyte Growth Factor, and Vascular Endothelial Growth Factor in Prostate Cancer Patients and Inhibit Production of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor In vitro

McLarty

Bigelow

Smith

et al. 2009

Cancer Prevention Research

227

167

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The purpose of this study was to determine the effects of short-term supplementation with the active compounds in green tea on serum biomarkers in patients with prostate cancer.Twenty-six men with positive prostate biopsies and scheduled for radical prostatectomy were given daily doses of Polyphenon E, which contained 800 mg of (−)-epigallocatechin-3-gallate (EGCG) and lesser amounts of (−)-epicatechin, (−)-epigallocatechin, and (−)-epicatechin-

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Section: Discussionmentioning

confidence: 87%

Tea Polyphenols Decrease Serum Levels of Prostate-Specific Antigen, Hepatocyte Growth Factor, and Vascular Endothelial Growth Factor in Prostate Cancer Patients and Inhibit Production of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor In vitro

McLarty

Bigelow

Smith

et al. 2009

Cancer Prevention Research

227

167

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“…There was one in vitro study, which showed that IGFIR antibodies inhibited DNA synthesis in PC3, but not DU145 cell lines [43]; however, other investigators found that IGFIR antibody prevents proliferation of both the prostate cell lines [44]. Although an association may exist between IGFI and prostate cancer, direct causality has not been established [45]. Another question is the role of VEGFR in autocrine growth regulation of prostate cells.…”

Section: Discussionmentioning

confidence: 99%

The effect of tyrosine kinase inhibitors, tyrphostins: AG1024 and SU1498, on autocrine growth of prostate cancer cells (DU145).

Kisielewska

Ligeza²,

Klein³

2008

Folia Histochem Cytobiol.

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Abstract:It is well established that autocrine growth of human prostate cancer cell line DU145 is dependent on TGF (EGF)/EGFR loop. However, the participation of several other growth factors in proliferation of DU145 cells has been also proposed. We employed two selective tyrosine kinase inhibitors (tyrphostins): AG1024 (an IGFIR inhibitor) and SU1498 (a VEGFR2 inhibitor) for growth regulation of DU145 cells, cultured in chemically defined DMEM/F12 medium. Both the tested compounds inhibited autocrine growth of DU145 cells at similar concentration values (IC50 ≈2.5 μM). The tyrphostins arrested cell growth of DU145 in G1 phase, similarly as inhibitors of EGFR. However, in contrast to selective inhibitors of EGFR, neither AG1024, nor SU1498 (at concentration ≤10 μM) decreased the viability of the investigated cells. These results strongly suggest that autocrine growth of DU145 cells is stimulated by, at least, three autocrine loops: TGFα(EGF)/EGFR, IGFII/IGFIr and VEGF/VEGFR2(VEGFR1). These data support the hypothesis of multi-loops growth regulation of metastatic prostate cancer cell lines.

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“…However, the role of IGF1 in adult animals is difficult to evaluate in these mice strains due to the possible effect of the absence of IGF1 activity during development. Moreover, there is a local production of IGF1 in the prostate (Kaplan et al 1999, Meinbach & Lokeshwar 2006, which is depleted in mice with global IGF1 knockout. By contrast, the LI-IGF1 K/K mice do not have decreased liver IGF1 expression until the inactivation K/K and control mice.…”

Section: Discussionmentioning

confidence: 99%

“…In primary culture, the prostatic epithelial cells express the IGF1 receptor and IGF1 stimulates them to proliferate and to produce IGFBPs into the medium (Perkel et al 1990, Cohen et al 1991. Prostatic stromal cells also express the IGF1 receptor (Cohen et al 1994a,b,c), and there is local production of IGF1 in these cells (Kaplan et al 1999, Meinbach & Lokeshwar 2006. The locally produced IGF1 from the stromal cells can act in a paracrine fashion on the prostatic epithelial cells (Meinbach & Lokeshwar 2006), which raises the possibility that locally produced IGF1, rather than circulating IGF1, could be important for prostate growth.…”

Section: Introductionmentioning

confidence: 99%

Liver-derived IGF1 enhances the androgenic response in prostate

Svensson

Kindblom²,

Shao³

et al. 2008

Journal of Endocrinology

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Both IGF1 and androgens are major enhancers of prostate growth and are implicated in the development of prostate hyperplasia and cancer. The aim of the present study was to investigate whether liver-derived endocrine IGF1 modulates the androgenic response in prostate. Mice with adult, liverspecific inactivation of IGF1 (LI-IGF1 K/K mice) displayed an w80% reduction in serum IGF1 levels associated with decreased prostate weight compared with control mice (anterior prostate lobe K19%, P!0 . 05; dorsolateral prostate (DLP) lobe K35%, P!0 . 01; ventral prostate (VP) lobe K47%, P!0 . 01). Reduced androgen receptor (Ar) mRNA and protein levels were observed in the VP lobe (K34% and K30% respectively, both P!0 . 05 versus control mice). Analysis of prostate morphology showed reductions in both the glandular and fibromuscular compartments of the VP and DLP lobes that were proportional to the reductions in the weights of these lobes. Immunohistochemistry revealed reduced intracellular AR immunoreactivity in the VP and DLP lobes. The non-aromatizable androgen dihydrotestosterone increased VP weight to a lesser extent in orchidectomized (ORX) LI-IGF1 K/K mice than in ORX controls (K40%, P!0 . 05 versus control mice). In conclusion, deficiency of liver-derived IGF1 reduces both the glandular and fibromuscular compartments of the prostate, decreases AR expression in prostate, and reduces the stimulatory effect of androgens on VP weight. These findings may explain, at least in part, the well-known clinical association between serum IGF1 levels and conditions with abnormal prostate growth.

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Insulin-like growth factors and their binding proteins in prostate cancer: Cause or consequence?☆

Cited by 48 publications

References 147 publications

Tea Polyphenols Decrease Serum Levels of Prostate-Specific Antigen, Hepatocyte Growth Factor, and Vascular Endothelial Growth Factor in Prostate Cancer Patients and Inhibit Production of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor In vitro

Tea Polyphenols Decrease Serum Levels of Prostate-Specific Antigen, Hepatocyte Growth Factor, and Vascular Endothelial Growth Factor in Prostate Cancer Patients and Inhibit Production of Hepatocyte Growth Factor and Vascular Endothelial Growth Factor In vitro

The effect of tyrosine kinase inhibitors, tyrphostins: AG1024 and SU1498, on autocrine growth of prostate cancer cells (DU145).

Liver-derived IGF1 enhances the androgenic response in prostate

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