Chikusetsusaponin IVa methyl ester induces cell cycle arrest by the inhibition of nuclear translocation of β-catenin in HCT116 cells

Biochem Biophys Res Commun. 2015 Apr 17;459(4):591-6. doi: 10.1016/j.bbrc.2015.02.152. Epub 2015 Mar 5.

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.

Keywords: Apoptosis; Cell cycle arrest; Chikusetsusaponin IVa methyl ester; Wnt; β-catenin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Cell Cycle / drug effects*
  • Cell Line
  • Cell Nucleus / metabolism*
  • DNA Primers
  • Esters / chemistry
  • Oleanolic Acid / analogs & derivatives*
  • Oleanolic Acid / chemistry
  • Oleanolic Acid / pharmacology
  • Protein Transport
  • Reverse Transcriptase Polymerase Chain Reaction
  • Saponins / chemistry
  • Saponins / pharmacology*
  • beta Catenin / metabolism*

Substances

  • DNA Primers
  • Esters
  • Saponins
  • beta Catenin
  • chikusetsu saponin IVa
  • Oleanolic Acid