Flavokawain A, a novel chalcone from kava extract, induces apoptosis in bladder cancer cells by involvement of Bax protein-dependent and mitochondria-dependent apoptotic pathway and suppresses tumor growth in mice

Cancer Res. 2005 Apr 15;65(8):3479-86. doi: 10.1158/0008-5472.CAN-04-3803.

Abstract

Consumption of the traditional kava preparation was reported to correlate with low and uncustomary gender ratios (more cancer in women than men) of cancer incidences in three kava-drinking countries: Fiji, Vanuatu, and Western Samoa. We have identified flavokawain A, B, and C but not the major kavalactone, kawain, in kava extracts as causing strong antiproliferative and apoptotic effect in human bladder cancer cells. Flavokawain A results in a significant loss of mitochondrial membrane potential and release of cytochrome c into the cytosol in an invasive bladder cancer cell line T24. These effects of flavokawain A are accompanied by a time-dependent decrease in Bcl-x(L), a decrease in the association of Bcl-x(L) to Bax, and an increase in the active form of Bax protein. Using the primary mouse embryo fibroblasts Bax knockout and wild-type cells as well as a Bax inhibitor peptide derived from the Bax-binding domain of Ku70, we showed that Bax protein was, at least in part, required for the apoptotic effect of flavokawain A. In addition, flavokawain A down-regulates the expression of X-linked inhibitor of apoptosis and survivin. Because both X-linked inhibitor of apoptosis and survivin are main factors for apoptosis resistance and are overexpressed in bladder tumors, our data suggest that flavokawain A may have a dual efficacy in induction of apoptosis preferentially in bladder tumors. Finally, the anticarcinogenic effect of flavokawain A was evident in its inhibitory growth of bladder tumor cells in a nude mice model (57% of inhibition) and in soft agar.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Carcinoma, Transitional Cell / drug therapy*
  • Carcinoma, Transitional Cell / pathology
  • Caspase 3
  • Caspase 9
  • Caspases / metabolism
  • Cell Growth Processes / drug effects
  • Chalcone / analogs & derivatives*
  • Chalcone / pharmacology*
  • Cytochromes c / metabolism
  • Flavonoids / pharmacology*
  • Humans
  • Inhibitor of Apoptosis Proteins
  • Kava / chemistry*
  • Membrane Potentials / drug effects
  • Mice
  • Mice, Nude
  • Microtubule-Associated Proteins / metabolism
  • Mitochondria / drug effects*
  • Mitochondria / physiology
  • Neoplasm Proteins
  • Plant Extracts / pharmacology
  • Poly(ADP-ribose) Polymerases / metabolism
  • Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Survivin
  • Urinary Bladder Neoplasms / drug therapy*
  • Urinary Bladder Neoplasms / pathology
  • X-Linked Inhibitor of Apoptosis Protein
  • Xenograft Model Antitumor Assays
  • bcl-2-Associated X Protein

Substances

  • BAX protein, human
  • BIRC5 protein, human
  • Bax protein, mouse
  • Flavonoids
  • Inhibitor of Apoptosis Proteins
  • Microtubule-Associated Proteins
  • Neoplasm Proteins
  • Plant Extracts
  • Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Survivin
  • X-Linked Inhibitor of Apoptosis Protein
  • XIAP protein, human
  • bcl-2-Associated X Protein
  • flavokawain A
  • flavokawain B
  • Chalcone
  • Cytochromes c
  • Poly(ADP-ribose) Polymerases
  • CASP3 protein, human
  • CASP9 protein, human
  • Casp3 protein, mouse
  • Casp9 protein, mouse
  • Caspase 3
  • Caspase 9
  • Caspases