We are analyzing https://link.springer.com/article/10.1007/s11095-011-0625-0.

Title:
Apigenin Attenuates Insulin-Like Growth Factor-I Signaling in an Autochthonous Mouse Prostate Cancer Model | Pharmaceutical Research
Description:
Purpose Deregulation of IGF signaling plays an important role in prostate cancer and contributes to invasion and metastasis. We determined the effect of apigenin, a plant flavone, on IGF signaling and its downstream targets in TRAMP mice. Methods Mice received p.o. apigenin at 20 and 50 μg/day dose for 20 weeks. ELISA, Western blotting and immunohistochemistry were performed to examine the IGF-axis and its regulated pathway in response to apigenin intake. Results Increased serum levels of IGF-I, VEGF, uPA and concomitant decrease in IGFBP-3 were observed; p-Akt (Ser473), p-ERK1 (T202/Y204) and p-ERK2 (T185/Y187) expression increased in the dorso-lateral prostate of TRAMP mice during the course of cancer progression as a function of age. P.o. administration of apigenin resulted in substantial reduction in the levels of IGF-I and increase in the levels of IGFBP-3 in the serum and the dorso-lateral prostate. This modulation of IGF/IGFBP-3 was associated with an inhibition of p-Akt and p-ERK1/2. Apigenin intake resulted in marked inhibition of VEGF, uPA, MMP-2 and MMP-9 which coincided with tumor growth inhibition and complete absence of metastasis in TRAMP mice. Conclusions Our results indicate that apigenin effectively suppressed prostate cancer progression in TRAMP mice by attenuating IGF-I/IGFBP-3 signaling and inhibiting angiogenesis and metastasis.
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Keywords {🔍}

cancer, article, prostate, google, scholar, pubmed, cas, growth, insulinlike, factor, apigenin, gupta, signaling, shukla, cell, res, mice, protein, research, metastasis, tramp, vegf, study, kinase, mouse, maclennan, receptor, usa, privacy, cookies, content, factori, model, sanjay, igf, intake, igfi, inhibition, angiogenesis, access, risk, int, case, cleveland, ohio, publish, search, autochthonous, pingfu, plant,

Topics {✒️}

growth factor-i-induced signaling month download article/chapter growth factor-binding protein-2 urokinase-type plasminogen activator protein-tyrosine kinase activity igf-binding protein-3 concentrations hypoxia-inducible factor-1-dependent related subjects pan-cancer analysis reveals autochthonous mouse model apigenin attenuates insulin wood research tower full article pdf growth factor-1 receptor protein kinase ck2 autochthonous prostate cancer growth factor axis privacy choices/manage cookies apigenin suppresses insulin benign prostatic hyperplasia human prostate cancer article shukla case–control study cell commun adhes prostate cancer detection prostate cancer cells author information authors natl cancer inst cancer metastasis rev dorso-lateral prostate prostate epithelium leads check access instant access prostate cancer risk phosphoinositide 3-kinase pathway cancer prev res prevent cancer foundation pi3k/akt pathway exp cell res dietary flavonoid intake clin endocrinol metab sanjay gupta european economic area 50 μg/day dose pharmacol exp ther food chem toxicol matrix-degrading proteases breast cancer risk growth factor growth factor 1

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

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         description:Deregulation of IGF signaling plays an important role in prostate cancer and contributes to invasion and metastasis. We determined the effect of apigenin, a plant flavone, on IGF signaling and its downstream targets in TRAMP mice. Mice received p.o. apigenin at 20 and 50 μg/day dose for 20 weeks. ELISA, Western blotting and immunohistochemistry were performed to examine the IGF-axis and its regulated pathway in response to apigenin intake. Increased serum levels of IGF-I, VEGF, uPA and concomitant decrease in IGFBP-3 were observed; p-Akt (Ser473), p-ERK1 (T202/Y204) and p-ERK2 (T185/Y187) expression increased in the dorso-lateral prostate of TRAMP mice during the course of cancer progression as a function of age. P.o. administration of apigenin resulted in substantial reduction in the levels of IGF-I and increase in the levels of IGFBP-3 in the serum and the dorso-lateral prostate. This modulation of IGF/IGFBP-3 was associated with an inhibition of p-Akt and p-ERK1/2. Apigenin intake resulted in marked inhibition of VEGF, uPA, MMP-2 and MMP-9 which coincided with tumor growth inhibition and complete absence of metastasis in TRAMP mice. Our results indicate that apigenin effectively suppressed prostate cancer progression in TRAMP mice by attenuating IGF-I/IGFBP-3 signaling and inhibiting angiogenesis and metastasis.
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      description:Deregulation of IGF signaling plays an important role in prostate cancer and contributes to invasion and metastasis. We determined the effect of apigenin, a plant flavone, on IGF signaling and its downstream targets in TRAMP mice. Mice received p.o. apigenin at 20 and 50 μg/day dose for 20 weeks. ELISA, Western blotting and immunohistochemistry were performed to examine the IGF-axis and its regulated pathway in response to apigenin intake. Increased serum levels of IGF-I, VEGF, uPA and concomitant decrease in IGFBP-3 were observed; p-Akt (Ser473), p-ERK1 (T202/Y204) and p-ERK2 (T185/Y187) expression increased in the dorso-lateral prostate of TRAMP mice during the course of cancer progression as a function of age. P.o. administration of apigenin resulted in substantial reduction in the levels of IGF-I and increase in the levels of IGFBP-3 in the serum and the dorso-lateral prostate. This modulation of IGF/IGFBP-3 was associated with an inhibition of p-Akt and p-ERK1/2. Apigenin intake resulted in marked inhibition of VEGF, uPA, MMP-2 and MMP-9 which coincided with tumor growth inhibition and complete absence of metastasis in TRAMP mice. Our results indicate that apigenin effectively suppressed prostate cancer progression in TRAMP mice by attenuating IGF-I/IGFBP-3 signaling and inhibiting angiogenesis and metastasis.
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         apigenin
         insulin-like growth factor
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         general
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         Biomedical Engineering and Bioengineering
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