Artículos de revistas
Anti-inflammatory Therapies In Tramp Mice: Delay In Prostate Cancer Progression.
Registro en:
Endocrine-related Cancer. v. 23, n. 4, 2016-Jan.
1479-6821
10.1530/ERC-15-0540
26772819
Autor
Kido, Larissa Akemi
Montico, Fabio
Sauce, Rafael
Macedo, Aline Barbosa
Minatel, Elaine
Vendramini Costa, Débora Barbosa
Carvalho, João Ernesto
Pilli, Ronaldo Aloise
Cagnon, Valeria
Institución
Resumen
The aim of this study was to evaluate the immediate and late responses of prostatic cancer in structural and molecular biology in the transgenic adenocarcinoma of the mouse prostate mice (TRAMP), after Goniothalamin and Celecoxib treatments. The treated mice received Goniothalamin (150mg/Kg, gavage) or Celecoxib (10mg/Kg, gavage) from 8 to 12 weeks of age, which were sacrificed at different ages; the immediate response groups at 12 weeks old and the late response groups at 22 weeks old. The ventral prostate was collected for light microscopy, immunohistochemistry, Western Blotting, TUNEL and ELISA. Morphological analyses indicated that Goniothalamin treatment delayed the prostatic adenocarcinoma progression, leading to a significant decrease of prostatic lesion frequency in both experimental period responses to this treatment, mainly high-grade prostatic intraepithelial neoplasia and well-differentiated adenocarcinoma. Also, the Celecoxib treatment showed a particular decrease in the proliferative processes (PCNA) in both experimental periods. Despite Celecoxib diminishing the COX2 and IGFR1 levels, Goniothalamin presented higher action spectrum considering the decrease of a greater molecular number involved in the proliferative and inflammatory processes in prostatic cancer. Goniothalamin attenuated the pro-inflammatory response in TRAMP prostatic microenvironment, delaying prostate cancer progression. Celecoxib treatment was efficient in the COX2 regulation in the TRAMP mice, mainly in the advanced disease grade. Finally, we concluded that inflammatory process control in prostate cancer early grades was crucial for the down regulation of the signaling pathways involved in the proliferative processes in advanced cancer grades. 23