Carregant...
Tipus de document
ArticleVersió
Versió publicadaData de publicació
Llicència de publicació
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/175002
Exenatide induces autophagy and prevents the cell regrowth in HepG2 cells
Títol de la revista
Director/Tutor
ISSN de la revista
Títol del volum
Recurs relacionat
Resum
The incidence of hepatocellular carcinoma (HCC) keeps rising year by year, and became the second leading cause of cancer-related death. Some studies have found that liraglutide, a GLP-1 analog, may decrease the tumor cells proliferation. Due to this, the aim of this work is to investigate the antiproliferative potential of exenatide, another GLP-1 analog. Cell proliferation was assessed by direct count with Trypan blue dye exclusion. Flow cytometry was used to determinate autophagy and nuclear staining. Morphometric analysis was used to verify senescence and apoptosis. The mechanism that induced cell growth inhibition was analyzed by Western Blot. Treatment with exenatide significantly decreases cell proliferation and increases autophagy, both in relation to control and liraglutide. In addition, mTOR inhibition was greater in cells treated with exenatide. In relation to chronic treatment, exenatide does not allow cellular regrowth by preventing some resistance mechanism that the cells can acquire. These results suggest that exenatide has a potent anti-proliferative activity via mTOR modulation and, among the GLP-1 analogs tested, could be in the future an alternative for HCC treatment.
Matèries (anglès)
Citació
Citació
CATYANA KRAUSE, Gabriele, GOULART LIMA, Kelly, LEVORSE, Vitor, VIEGAS HAUTE, Gabriela, BENEDETTI GASSEN, Rodrigo, GARCIA, Maria claudia, PEDRAZZA, Leonardo, FAGUNDES DONADIO, Marcio vinicius, LUFT, Carolina, RODRIGUES DE OLIVEIRA, Jarbas. Exenatide induces autophagy and prevents the cell regrowth in HepG2 cells. _EXCLI Journal 2019_. vol.18. Vol. 540-548. [consulta: 21 de gener de 2026]. ISSN: 1611-2156. [Disponible a: https://hdl.handle.net/2445/175002]