Chikusetsusaponin IVa methyl ester induces cell cycle arrest by the inhibition of nuclear translocation of b-catenin in HCT116 cells
- Chikusetsusaponin IVa methyl ester induces cell cycle arrest by the inhibition of nuclear translocation of b-catenin in HCT116 cells
- 이경미; 윤지호; 이동화; 박영균; 손근호; 노주원; 김영식
- Apoptosis; Chikusetsusaponin IVa methyl ester; Cell cycle arrest; Wnt; β-catenin
- Issue Date
- Biochemical and biophysical research communications
- VOL 459, 591-596
- 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
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