Induction of sestrin 2 is associated with fisetin-mediated apoptosis in human head and neck cancer cell lines.
apoptosis
fisetin
human head and neck cancer
sestrin 2
Journal
Journal of clinical biochemistry and nutrition
ISSN: 0912-0009
Titre abrégé: J Clin Biochem Nutr
Pays: Japan
ID NLM: 8700907
Informations de publication
Date de publication:
Mar 2019
Mar 2019
Historique:
received:
05
06
2018
accepted:
23
07
2018
entrez:
3
4
2019
pubmed:
3
4
2019
medline:
3
4
2019
Statut:
ppublish
Résumé
Fisetin was reported to have an anti-proliferative and apoptotic activity as a novel anti-cancer agent in various cancer cell lines. However, the possible molecular targets for the anti-cancer effect of fisetin in human head and neck cancer (HNCC) have not yet been clarified. In this study, the influence of fisetin on the growth and apoptosis of HNCCs were examined. In HSC3 cells, fisetin treatment reduced the viability and induced apoptosis. Through the results from the screening of the expression profile of apoptosis-related genes, sestrin 2 (SESN2) was functionally involved in fisetin-mediated apoptosis showing the knockdown of SESN2 by siRNA clearly restored fisetin-induced apoptosis. In addition, fisetin reduced the protein expression levels of phospho-mTOR (p-mTOR) and Mcl-1, which are the downstream molecules of SESN2. It also induced PARP cleavage by inducing an increase in the expression levels of SESN2 together with reducing mTOR and Mcl-1 proteins in other three HNCCs (MC3, Ca9.22, and HN22). Taken together, our findings suggest that the anti-cancer effect of fisetin on HNCCs is associated with SESN2/mTOR/Mcl-1 signaling axis.
Identifiants
pubmed: 30936621
doi: 10.3164/jcbn.18-63
pii: jcbn18-63
pmc: PMC6436036
doi:
Types de publication
Journal Article
Langues
eng
Pagination
97-105Déclaration de conflit d'intérêts
No potential conflicts of interest were disclosed.
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