Actualización del papel de la quimioterapia endovesical en el cáncer de vejiga no músculo-invasivo

Unda, Miguel; Fernandez-Gomez, Jesus; Cozar-Olmos, J.M.; Juárez, A.; Palou, Juan; Martínez‐Piñeiro, Luis

doi:10.1016/j.acuro.2017.09.006

Cited by 5 publications

(1 citation statement)

References 17 publications

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“…Although the prognosis after TUR is good and the 5-year survival rate is at least 95%, the high recurrence rate is a clinical problem [ 2 ]. Treatment with anticancer agents [ 3 , 4 ] and bacillus Calmette-Guérin (BCG) infusion [ 5 , 6 ] into the bladder are performed after TUR. However, these treatments impose both a heavy burden on the patient and a large economic burden [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

A Mechanism by which Ergosterol Inhibits the Promotion of Bladder Carcinogenesis in Rats

et al. 2020

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We previously showed that ergosterol has an inhibitory effect on bladder carcinogenesis. In this study, we aimed to elucidate the molecular mechanism by which ergosterol inhibits bladder carcinogenesis using a rat model of N-butyl-N-(4-hydroxybutyl)nitrosamine-induced bladder cancer. The messenger ribonucleic acid (mRNA) expression level of the cell cycle-related gene cyclin D1 and inflammation-related gene cyclooxygenase-2 in bladder epithelial cells was significantly increased in the carcinogenesis group compared with the control group. In contrast, in ergosterol-treated rats, these increases were significantly suppressed. Ergosterol did not affect the plasma testosterone concentration or the binding of dihydrotestosterone to androgen receptor (AR). The mRNA expression levels of 5α-reductase type 2 and AR were higher in the carcinogenesis group than in the control group but were significantly decreased by ergosterol administration. These results suggest that ergosterol inhibits bladder carcinogenesis by modulating various aspects of the cell cycle, inflammation-related signaling, and androgen signaling. Future clinical application of the preventive effect of ergosterol on bladder carcinogenesis is expected.

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Section: Introductionmentioning

confidence: 99%

A Mechanism by which Ergosterol Inhibits the Promotion of Bladder Carcinogenesis in Rats

et al. 2020

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Mechanistic analysis of bladder cancer suppression by brassicasterol in a rat model of N‐butyl‐N‐(4‐hydroxybutyl)nitrosamine‐induced bladder cancer

Ikarashi

Ono

Hoshino

et al. 2021

Traditional & Kampo Medicine

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Aim We previously clarified that the herbal medicine Polyporus Sclerotium, a constituent of Choreito, has an inhibitory effect on bladder carcinogenesis and that ergosterol is the active ingredient. In addition, we showed that this action of ergosterol may be caused by the metabolite brassicasterol. Here, we aimed to elucidate the detailed molecular mechanism by which brassicasterol inhibits bladder carcinogenesis. Methods A rat model of bladder cancer was established by feeding rats N‐butyl‐N‐(4‐hydroxybutyl)nitrosamine (BHBN) and sodium saccharin (SS). After intraperitoneal administration of brassicasterol to rats, the mRNA expression levels of cell cycle‐related genes (cyclin D1, c‐fos, and c‐jun), inflammation‐related genes (cyclooxygenase‐2; COX‐2), and androgen signal‐related genes (5α‐reductase type 1; 5α‐R1, 5α‐reductase type 2; 5α‐R2, and the androgen receptor; AR) in bladder epithelial cells were analyzed. Results Brassicasterol significantly suppressed bladder carcinogenesis induced by BHBN and SS. The mRNA expression levels of cyclin D1 in bladder epithelial cells were significantly higher in the carcinogenesis group than in the control group. Additionally, the expression levels of c‐fos and c‐jun, constituents of the transcription factor activator protein‐1 (AP‐1) upstream of cyclin D1, were significantly increased in the carcinogenesis group compared with the control group. Moreover, the expression levels of COX‐2, 5α‐R1, 5α‐R2, and AR were significantly higher in the carcinogenesis group. In contrast, in rats treated with brassicasterol, the increases in the expression levels of these molecules were significantly suppressed. Conclusion We clarified that brassicasterol suppresses bladder carcinogenesis by acting on cell cycle‐related signaling, inflammation‐related signaling, and androgen signaling via multiple mechanisms.

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Inhibitory effect of ergosterol on bladder carcinogenesis is due to androgen signaling inhibition by brassicasterol, a metabolite of ergosterol

et al. 2020

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Actualización del papel de la quimioterapia endovesical en el cáncer de vejiga no músculo-invasivo

Cited by 5 publications

References 17 publications

A Mechanism by which Ergosterol Inhibits the Promotion of Bladder Carcinogenesis in Rats

A Mechanism by which Ergosterol Inhibits the Promotion of Bladder Carcinogenesis in Rats

Mechanistic analysis of bladder cancer suppression by brassicasterol in a rat model of N‐butyl‐N‐(4‐hydroxybutyl)nitrosamine‐induced bladder cancer

Inhibitory effect of ergosterol on bladder carcinogenesis is due to androgen signaling inhibition by brassicasterol, a metabolite of ergosterol

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