IMR Press / FBE / Volume 3 / Issue 4 / DOI: 10.2741/E335

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Sanggenon C decreases tumor cell viability associated with proteasome inhibition
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1 Protein Modification and degradation Lab, Department of Pathophysiology
2 The Developmental Therapeutics Program, Barbara Ann Karmanos Cancer Institute, and Departments of Oncology, Pharmacology and Pathology, School of Medicine, Wayne State University. Detroit, Michigan, USA
3 School of Chinese Medicine, Guangzhou University of Traditional Chinese Medicine. Guangzhou, Guangdong, People’s Republic of China
4 Division of Biomedical Sciences, University of South Dakota Sanford School of Medicine, Vermillion, South Dakota, USA

*Author to whom correspondence should be addressed.

Academic Editor: Hala Gali-Muhtasib

Front. Biosci. (Elite Ed) 2011, 3(4), 1315–1325; https://doi.org/10.2741/E335
Published: 1 June 2011
(This article belongs to the Special Issue New emerging anticancer lead compounds from plants)
Abstract

Several flavonoids have been reported to be proteasome inhibitors, but whether prenylated flavonoids are able to inhibit proteasome function remains unknown. We report for the first time that Sanggenon C, a natural prenylated flavonoid, inhibits tumor cellular proteasomal activity and cell viability. We found that (1) Sanggenon C inhibited tumor cell viability and induced cell cycle arrest at G0/G1 phase; (2) Sanggenon C inhibited the chymotrypsin-like activity of purified human 20S proteasome and 26S proteasome in H22 cell lysate, and Sanggenon C was able to dose-dependently accumulate ubiquitinated proteins and proteasome substrate protein p27; (3) Sanggenon C-induced proteasome inhibition occurred prior to cell death in murine H22 and P388 cell lines; (4) Sanggenon C induced death of human K562 cancer cells and primary cells isolated from leukemic patients. We conclude that Sanggenon C inhibits tumor cell viability via induction of cell cycle arrest and cell death, which is associated with its ability to inhibit the proteasome function and that proteasome inhibition by Sanggenon C at least partially contributes to the observed tumor cell growth-inhibitory activity.

Keywords
Sanggenon C
proteasome inhibitor
cell death
cell cycle
flavonoid
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