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Author Lee, Kyung-Mi ♦ Yun, Ji Ho ♦ Lee, Dong Hwa ♦ Park, Young Gyun ♦ Son, Kun Ho ♦ Nho, Chu Won ♦ Kim, Yeong Shik
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ APOPTOSIS ♦ CELL CYCLE ♦ CELL PROLIFERATION ♦ DEPTH ♦ DNA ♦ ESTERS ♦ GENES ♦ INHIBITION ♦ NEOPLASMS ♦ PROMOTERS ♦ PROTEINS ♦ SAPONINS
Abstract We demonstrate that chikusetsusaponin IVa methyl ester (CME), a triterpenoid saponin from the root of Achyranthes japonica, has an anticancer activity. We investigate its molecular mechanism in depth in HCT116 cells. CME reduces the amount of β-catenin in nucleus and inhibits the binding of β-catenin to specific DNA sequences (TCF binding elements, TBE) in target gene promoters. Thus, CME appears to decrease the expression of cell cycle regulatory proteins such as Cyclin D1, as a representative target for β-catenin, as well as CDK2 and CDK4. As a result of the decrease of the cell cycle regulatory proteins, CME inhibits cell proliferation by arresting the cell cycle at the G0/G1 phase. Therefore, we suggest that CME as a novel Wnt/β-catenin inhibitor can be a putative agent for the treatment of colorectal cancers. - Highlights: • CME inhibits cell proliferation in HCT116 cells. • CME increases cell cycle arrest at G0/G1 phase and apoptosis. • CME attenuates cyclin D1 and regulates cell cycle regulatory proteins. • CME inhibits β-catenin translocation to nucleus.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-04-17
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 459
Issue Number 4


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