Ganoderic acids suppress growth and invasive behavior of breast cancer cells by modulating AP-1 and NF-κB signaling

  • Authors:
    • Jiahua Jiang
    • Brian Grieb
    • Anita Thyagarajan
    • Daniel Sliva
  • View Affiliations

  • Published online on: May 1, 2008     https://doi.org/10.3892/ijmm.21.5.577
  • Pages: 577-584
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Abstract

Structurally related lanostane-type triterpenes, ganoderic acid A, F and H (GA-A, GA-F, GA-H), were identified in an oriental medicinal mushroom Ganoderma lucidum. In the present study we evaluated the effect of GA-A, GA-H and GA-F on highly invasive human breast cancer cells. We showed that GA-A and GA-H suppressed growth (cell proliferation and colony formation) and invasive behavior (adhesion, migration and invasion) of MDA-MB-231 cells. Our results suggest that GA-A and GA-H mediate their biological effects through the inhibition of transcription factors AP-1 and NF-κB, resulting in the down-regulation of expression of Cdk4 and the suppression of secretion of uPA, respectively. Furthermore, the activity of ganoderic acids is linked to the hydroxylation in the position 7 and 15 (GA-A) and 3 (GA-H) in their triterpene lanostane structure. In conclusion, hydroxylated triterpenes from G. lucidum could be promising natural agents for the therapy of invasive breast cancers.

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May 2008
Volume 21 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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APA
Jiang, J., Grieb, B., Thyagarajan, A., & Sliva, D. (2008). Ganoderic acids suppress growth and invasive behavior of breast cancer cells by modulating AP-1 and NF-κB signaling. International Journal of Molecular Medicine, 21, 577-584. https://doi.org/10.3892/ijmm.21.5.577
MLA
Jiang, J., Grieb, B., Thyagarajan, A., Sliva, D."Ganoderic acids suppress growth and invasive behavior of breast cancer cells by modulating AP-1 and NF-κB signaling". International Journal of Molecular Medicine 21.5 (2008): 577-584.
Chicago
Jiang, J., Grieb, B., Thyagarajan, A., Sliva, D."Ganoderic acids suppress growth and invasive behavior of breast cancer cells by modulating AP-1 and NF-κB signaling". International Journal of Molecular Medicine 21, no. 5 (2008): 577-584. https://doi.org/10.3892/ijmm.21.5.577