Abstract
Original language | English |
---|---|
Pages (from-to) | 759-777 |
Number of pages | 19 |
Journal | Endocrine-Related Cancer |
Volume | 19 |
Issue number | 6 |
DOIs | |
Publication status | Published - Dec 2012 |
Externally published | Yes |
Keywords
- daidzein
- filamin A
- genistein
- polysaccharide
- advanced cancer
- androgen deprivation therapy
- animal experiment
- animal model
- apoptosis
- article
- cancer recurrence
- castration
- cell cycle arrest
- controlled study
- human
- human cell
- male
- mouse
- nonhuman
- prostate cancer
- protein phosphorylation
- tumor xenograft
- Androgen Antagonists
- Androgens
- Anilides
- Animals
- Apoptosis
- Castration
- Cell Cycle Checkpoints
- Cell Line, Tumor
- Cell Nucleus
- Filamins
- Genistein
- Male
- Mice
- Mice, Nude
- Nitriles
- Polysaccharides
- Prostatic Neoplasms
- Tosyl Compounds
- Tumor Burden
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Enhancing the effectiveness of androgen deprivation in prostate cancer by inducing Filamin A nuclear localization. / Mooso, B.A.; Vinall, R.L.; Tepper, C.G. et al.
In: Endocrine-Related Cancer, Vol. 19, No. 6, 12.2012, p. 759-777.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Enhancing the effectiveness of androgen deprivation in prostate cancer by inducing Filamin A nuclear localization
AU - Mooso, B.A.
AU - Vinall, R.L.
AU - Tepper, C.G.
AU - Savoy, R.M.
AU - Cheung, J.P.
AU - Singh, S.
AU - Siddiqui, S.
AU - Wang, Y.
AU - Bedolla, R.G.
AU - Martinez, A.
AU - Mudryj, M.
AU - Kung, H.-J.
AU - DeVere White, R.W.
AU - Ghosh, P.M.
N1 - 引用次數:13 Export Date: 5 March 2018 CODEN: ERCAE 通訊地址: Ghosh, P.M.; Department of Urology, University of California Davis School of Medicine, 4860 Y Street, Sacramento, CA 95817, United States; 電子郵件: paramita.ghosh@ucdmc.ucdavis.edu 化學物質/CAS: daidzein, 486-66-8; genistein, 446-72-0; Androgen Antagonists; Androgens; Anilides; Filamins; FlnA protein, mouse; Genistein, DH2M523P0H; Nitriles; Polysaccharides; Tosyl Compounds; bicalutamide, 90357-06-5; genistein combined polysaccharide 參考文獻: Aggarwal, B.B., Shishodia, S., Molecular targets of dietary agents for prevention and therapy of cancer (2006) Biochemical Pharmacology, 71, pp. 1397-1421. , doi:10.1016/j.bcp.2006.02.009; Agus, D.B., Cordon-Cardo, C., Fox, W., Drobnjak, M., Koff, A., Golde, D.W., Scher, H.I., Prostate cancer cell cycle regulators: Response to androgen withdrawal and development of androgen independence (1999) Journal of the National Cancer Institute, 91, pp. 1869-1876. , doi:10.1093/jnci/91.21.1869; Agus, D.B., Akita, R.W., Fox, W.D., Lewis, G.D., Higgins, B., Pisacane, P.I., Lofgren, J.A., Maiese, K., Targeting ligand-activated ErbB2 signaling inhibits breast and prostate tumor growth (2002) Cancer Cell, 2, pp. 127-137. , doi:10.1016/S1535-6108(02)00097-1; 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PY - 2012/12
Y1 - 2012/12
N2 - As prostate cancer (CaP) is regulated by androgen receptor (AR) activity, metastatic CaP is treated with androgen deprivation therapy (ADT). Despite initial response, patients on ADT eventually progress to castration-resistant CaP (CRPC), which is currently incurable. We previously showed that cleavage of the 280 kDa structural protein Filamin A (FlnA) to a 90 kDa fragment, and nuclear localization of the cleaved product, sensitized CRPC cells to ADT. Hence, treatment promoting FlnA nuclear localization would enhance androgen responsiveness. Here, we show that FlnA nuclear localization induced apoptosis in CRPC cells during ADT, identifying it as a treatment tool in advanced CaP. Significantly, the natural product genistein combined polysaccharide (GCP) had a similar effect. Investigation of the mechanism of GCP-induced apoptosis showed that GCP induced FlnA cleavage and nuclear localization and that apoptosis resulting from GCP treatment was mediated by FlnA nuclear localization. Two main components of GCP are genistein and daidzein: the ability of GCP to induce G2 arrest was due to genistein whereas sensitivity to ADT stemmed from daidzein; hence, both were needed to mediate GCP's effects. FlnA cleavage is regulated by its phosphorylation; we show that ADT enhanced FlnA phosphorylation, which prevented its cleavage, whereas GCP inhibited FlnA phosphorylation, thereby sensitizing CaP cells to ADT. In a mouse model of CaP recurrence, GCP, but not vehicle, impeded relapse following castration, indicating that GCP, when administered with ADT, interrupted the development of CRPC. These results demonstrate the efficacy of GCP in promoting FlnA nuclear localization and enhancing androgen responsiveness in CaP. © 2012 Society for Endocrinology.
AB - As prostate cancer (CaP) is regulated by androgen receptor (AR) activity, metastatic CaP is treated with androgen deprivation therapy (ADT). Despite initial response, patients on ADT eventually progress to castration-resistant CaP (CRPC), which is currently incurable. We previously showed that cleavage of the 280 kDa structural protein Filamin A (FlnA) to a 90 kDa fragment, and nuclear localization of the cleaved product, sensitized CRPC cells to ADT. Hence, treatment promoting FlnA nuclear localization would enhance androgen responsiveness. Here, we show that FlnA nuclear localization induced apoptosis in CRPC cells during ADT, identifying it as a treatment tool in advanced CaP. Significantly, the natural product genistein combined polysaccharide (GCP) had a similar effect. Investigation of the mechanism of GCP-induced apoptosis showed that GCP induced FlnA cleavage and nuclear localization and that apoptosis resulting from GCP treatment was mediated by FlnA nuclear localization. Two main components of GCP are genistein and daidzein: the ability of GCP to induce G2 arrest was due to genistein whereas sensitivity to ADT stemmed from daidzein; hence, both were needed to mediate GCP's effects. FlnA cleavage is regulated by its phosphorylation; we show that ADT enhanced FlnA phosphorylation, which prevented its cleavage, whereas GCP inhibited FlnA phosphorylation, thereby sensitizing CaP cells to ADT. In a mouse model of CaP recurrence, GCP, but not vehicle, impeded relapse following castration, indicating that GCP, when administered with ADT, interrupted the development of CRPC. These results demonstrate the efficacy of GCP in promoting FlnA nuclear localization and enhancing androgen responsiveness in CaP. © 2012 Society for Endocrinology.
KW - daidzein
KW - filamin A
KW - genistein
KW - polysaccharide
KW - advanced cancer
KW - androgen deprivation therapy
KW - animal experiment
KW - animal model
KW - apoptosis
KW - article
KW - cancer recurrence
KW - castration
KW - cell cycle arrest
KW - controlled study
KW - human
KW - human cell
KW - male
KW - mouse
KW - nonhuman
KW - prostate cancer
KW - protein phosphorylation
KW - tumor xenograft
KW - Androgen Antagonists
KW - Androgens
KW - Anilides
KW - Animals
KW - Apoptosis
KW - Castration
KW - Cell Cycle Checkpoints
KW - Cell Line, Tumor
KW - Cell Nucleus
KW - Filamins
KW - Genistein
KW - Male
KW - Mice
KW - Mice, Nude
KW - Nitriles
KW - Polysaccharides
KW - Prostatic Neoplasms
KW - Tosyl Compounds
KW - Tumor Burden
U2 - 10.1530/ERC-12-0171
DO - 10.1530/ERC-12-0171
M3 - Article
SN - 1351-0088
VL - 19
SP - 759
EP - 777
JO - Endocrine-Related Cancer
JF - Endocrine-Related Cancer
IS - 6
ER -