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Mechanism of cis-Nerolidol-Induced Bladder Carcinoma Cell Death (CROSBI ID 321302)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Glumac, Mateo ; Čikeš Čulić, Vedrana ; Marinović-Terzić, Ivana ; Radan, Mila Mechanism of cis-Nerolidol-Induced Bladder Carcinoma Cell Death // Cancers, 15 (2023), 3; 15030981, 20. doi: 10.3390/cancers15030981

Podaci o odgovornosti

Glumac, Mateo ; Čikeš Čulić, Vedrana ; Marinović-Terzić, Ivana ; Radan, Mila

engleski

Mechanism of cis-Nerolidol-Induced Bladder Carcinoma Cell Death

Nerolidol is a naturally occurring sesquiterpene alcohol with multiple properties, including antioxidant, antibacterial, and antiparasitic activities. A few studies investigating the antitumor properties of nerolidol have shown positive results in both cell culture and mouse models. In this study, we investigated the antitumor mechanism of cis-nerolidol in bladder carcinoma cell lines. The results of our experiments on two bladder carcinoma cell lines revealed that nerolidol inhibited cell proliferation and induced two distinct cell death pathways. We confirmed that cis-nerolidol induces DNA damage and ER stress. A mechanistic study identified a common cAMP, Ca2+, and MAPK axis involved in signal propagation and amplification, leading to ER stress. Inhibition of any part of this signaling cascade prevented both cell death pathways. The two cell death mechanisms can be distinguished by the involvement of caspases. The early occurring cell death pathway is characterized by membrane blebbing and cell swelling followed by membrane rupture, which can be prevented by the inhibition of caspase activation. In the late cell death pathway, which was found to be caspase-independent, cytoplasmic vacuolization and changes in cell shape were observed. cis-Nerolidol shows promising antitumor activity through an unorthodox mechanism of action that could help target resistant forms of malignancies, such as bladder cancer.

nerolidol ; sesquiterpenes ; cell death pathways ; calcium signaling ; ER stress

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Podaci o izdanju

15 (3)

2023.

15030981

20

objavljeno

2072-6694

10.3390/cancers15030981

Povezanost rada

Biologija, Farmacija, Interdisciplinarne prirodne znanosti, Kemija

Poveznice
Indeksiranost