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Compound K induces apoptosis via CAMK-IV/AMPK pathways in HT-29 colon cancer cells

Do Yeon Kim1, Min Woo Park, Hai Dan Yuan

  • 1Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 130-701, Korea.

Journal of Agricultural and Food Chemistry
|October 23, 2009
PubMed

Insights

Compound K (CK) triggers apoptosis in colon cancer cells by activating the Ca2+/calmodulin-dependent protein kinase-IV (CAMK-IV) and AMP-activated protein kinase (AMPK) pathways, offering a molecular basis for its anticancer effects.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Oncology

Background:

  • Compound K (CK), a ginseng metabolite, induces apoptosis in cancer cells.
  • The role of AMP-activated protein kinase (AMPK) in CK-induced apoptosis in HT-29 colon cancer cells is not fully understood.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying CK's anticancer activity in HT-29 colon cancer cells.
  • To determine if the AMPK pathway is involved in CK-induced apoptosis.

Main Methods:

  • HT-29 cells were treated with Compound K.
  • Apoptosis was assessed by measuring mitochondrial membrane potential, cytochrome c release, and caspase cleavage.
  • AMPK activation was analyzed via Western blotting and inhibited using Compound C or siRNA.
  • Ca2+/calmodulin-dependent protein kinase-IV (CAMK-IV) was inhibited using STO-609.

Main Results:

  • CK induced apoptosis in HT-29 cells, evidenced by mitochondrial dysfunction and caspase activation.
  • CK treatment led to the activation of AMPK.
  • AMPK activation was dependent on CAMK-IV.
  • Inhibition of AMPK or CAMK-IV abrogated CK-induced apoptosis.

Conclusions:

  • CK-induced apoptosis in HT-29 colon cancer cells is mediated through the CAMK-IV/AMPK signaling pathway.
  • These findings elucidate the molecular mechanisms of CK's anticancer effects and suggest its therapeutic potential.

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