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001-es BibID:BIBFORM009099
Első szerző:Czifra Gabriella (élettanász)
Cím:Increased expressions of cannabinoid receptor-1 and transient receptor potential vanilloid-1 in human prostate carcinoma / Czifra, G., Varga, A., Nyeste, K., Marincsak, R., Toth, B. I., Kovacs, I., Kovacs, L., Biro, T.
Dátum:2009
ISSN:0171-5216
Megjegyzések:Recently, functional cannabinoid receptor-1 (CB1) and vanilloid receptor-1 (TRPV1) have been described in human prostate and prostate cancer-derived cell lines where the activation of the receptors resulted in inhibition of cellular growth. We, however, lack the description of the expression of these molecules in human prostate cancer (PCC) and in benign prostate hyperplasia (BPH). METHODS: Therefore, immunohistochemistry, Western blotting, and quantitative "real-time Q-PCR were performed to define the expressions of CB1 and TRPV1 in healthy and diseased prostate tissues. RESULTS: CB1 was identified in epithelial and smooth muscle cells types of the human prostate, whereas TRPV1 was exclusively localized to the mucosal cells. We also found that the expression of CB1 and TRPV1 (both at the protein and mRNA levels) were significantly up-regulated in PCC. However, while the increased expression of TRPV1 showed a proper correlation with increasing PCC tumor grades, such phenomenon was not observed with CB1. In addition, we also measured markedly elevated CB1 levels in BPH tissues whilst the expression of TRPV1 was not altered when compared to healthy control prostate. CONCLUSIONS: Our findings strongly argue for that (1) the CB1 and TRPV1 molecules as well as their ligands may indeed possess a promising future role in the treatment of PCC; (2) TRPV1 may also serve as a prognostic factor in PCC; and (3) CB1 may act as a potential target molecule in the therapeutic management of BPH.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Cancer Research and Clinical Oncology. - 135 : 4 (2009), p. 507-514. -
További szerzők:Varga Attila (1949-) (urológus, andrológus) Nyeste Katalin Marincsák Rita (1979-) (fogszakorvos) Tóth István Balázs (1978-) (élettanász) Kovács Ilona (1965-) (patológus) Kovács László (1939-) (élettanász) Bíró Tamás (1968-) (élettanász)
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001-es BibID:BIBFORM015638
Első szerző:Yang, Dazhi
Cím:RasGRP3 Contributes to Formation and Maintenance of the Prostate Cancer Phenotype / Yang, D., Kedei, N., Li, L., Tao, J., Velasquez, J. F., Michalowski, A. M., Toth, B. I., Marincsak, R., Varga, A., Biro, T., Yuspa, S. H., Blumberg, P. M.
Dátum:2010
ISSN:0008-5472
Megjegyzések:RasGRP3 mediates the activation of the Ras signaling pathway that is present in many human cancers. Here, we explored the involvement of RasGRP3 in the formation and maintenance of the prostate cancer phenotype. RasGRP3 expression was elevated in multiple human prostate tumor tissue samples and in the human androgen-independent prostate cancer cell lines PC-3 and DU 145 compared with the androgen-dependent prostate cancer cell line LNCaP. Downregulation of endogenous RasGRP3 in PC-3 and DU 145 cells reduced Ras-GTP formation, inhibited cell proliferation, impeded cell migration, and induced apoptosis. Anchorage-independent growth of the PC-3 cells and tumor formation in mouse xenografts of both cell lines were likewise inhibited. Inhibition of RasGRP3 expression reduced AKT and extracellular signal-regulated kinase 1/2 phosphorylation and sensitized the cells to killing by carboplatin. Conversely, exogenous RasGRP3 elevated Ras-GTP, stimulated proliferation, and provided resistance to phorbol 12-myristate 13-acetate-induced apoptosis in LNCaP cells. RasGRP3-overexpressing LNCaP cells displayed a markedly enhanced rate of xenograft tumor formation in both male and female mice compared with the parental line. Suppression of RasGRP3 expression in these cells inhibited downstream RasGRP3 responses, caused the cells to resume the LNCaP morphology, and suppressed growth, confirming the functional role of RasGRP3 in the altered behavior of these cells. We conclude that RasGRP3 contributes to the malignant phenotype of the prostate cancer cells and may constitute a novel therapeutic target for human prostate cancer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cancer Research. - 70 : 20 (2010), p. 7905-7917. -
További szerzők:Kedei Noémi Li, Luowei Tao, Juan Velasquez, Julia F. Michalowski, Aleksandra M. Tóth István Balázs (1978-) (élettanász) Marincsák Rita (1979-) (fogszakorvos) Varga Attila (1949-) (urológus, andrológus) Bíró Tamás (1968-) (élettanász) Yuspa, Stuart H. Blumberg, Peter M.
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