Please use this identifier to cite or link to this item: http://hdl.handle.net/10400.11/5737
Title: Urolithins impair cell proliferation, arrest the cell cycle and induce apoptosis in UMUC3 bladder cancer cells
Author: Liberal, Joana
Carmo, Anália
Gomes, Célia
Cruz, Maria Teresa
Batista, Maria Teresa
Keywords: Apoptosis
Cell cycle
Ellagitannins
Intracellular signaling pathways
UMUC3
Urolithins
Issue Date: 20-Jul-2017
Publisher: Springer US
Citation: Liberal, J., Carmo, A., Gomes, C. et al. Urolithins impair cell proliferation, arrest the cell cycle and induce apoptosis in UMUC3 bladder cancer cells. Invest New Drugs (2017). https://doi.org/10.1007/s10637-017-0483-7
Abstract: Ellagitannins have been gaining attention as potential anticancer molecules. However, the low bioavailability of ellagitannins and their extensive metabolization in the gastrointestinal tract into ellagic acid and urolithins suggest that the health benefits of consuming ellagitannins rely on the direct effects of their metabolites. Recently, chemopreventive and chemotherapeutic activities were ascribed to urolithins. Nonetheless, there is still a need to screen and evaluate the selectivity of these molecules and to elucidate their cellular mechanisms of action. Therefore, this work focused on the antiproliferative effects of urolithins A, B and C and ellagic acid on different human tumor cell lines. The evaluation of cell viability and the determination of the half-maximal inhibitory concentrations indicated that the sensitivity to the studied urolithins varied markedly between the different cell lines, with the bladder cancer cells (UMUC3) being the most susceptible. In UMUC3 cells, urolithin A was the most active molecule, promoting cell cycle arrest at the G2/M checkpoint, increasing apoptotic cell death and inhibiting PI3K/Akt and MAPK signaling. Overall, the present study emphasizes the chemopreventive/chemotherapeutic potential of urolithins, highlighting the stronger effects of urolithin A and its potential to target transitional bladder cancer cells.
Peer review: yes
URI: http://hdl.handle.net/10400.11/5737
DOI: 10.1007/s10637-017-0483-7
ISSN: 0167-6997
Publisher Version: https://link.springer.com/article/10.1007%2Fs10637-017-0483-7
Appears in Collections:ESALD - Artigos em revistas com arbitragem científica

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