Inhibition of prostatic cancer growth by ginsenoside Rh2

Tumour Biol. 2015 Apr;36(4):2377-81. doi: 10.1007/s13277-014-2845-5. Epub 2014 Nov 23.


Ginsenoside Rh2 (GRh2) has been reported to have therapeutic effects on some types of cancer, but its effect on prostatic cancer has not been extensively evaluated. Here, we show that GRh2 can substantially inhibit the growth of prostatic cancer in vivo and in vitro. Moreover, the inhibition of the tumor growth appeared to result from a combined inhibitory effect on tumor cell proliferation and tumor cell invasiveness. Further analyses suggest that GRh2 seemed to activate transforming growth factor β (TGFβ) receptor signaling in prostatic cancer cells, which subsequently inhibits cell proliferation and invasion through regulating cell-cycle controllers and (MMPs), respectively. Taken together, our data reveal an essential anti-prostatic cancer effect of GRh2 and demonstrate that this effect is through augment of TGFβ receptor signaling in the prostatic cancer cells. GRh2 thus appears to be a promising therapy for prostatic cancer.

MeSH terms

  • Animals
  • Apoptosis
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Gene Expression Regulation, Neoplastic / genetics
  • Ginsenosides / administration & dosage*
  • Ginsenosides / genetics
  • Humans
  • Male
  • Mice
  • Neoplasm Invasiveness / genetics
  • Neoplasm Proteins / biosynthesis
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology
  • Receptors, Transforming Growth Factor beta / biosynthesis*
  • Receptors, Transforming Growth Factor beta / genetics
  • Signal Transduction / drug effects


  • Ginsenosides
  • Neoplasm Proteins
  • Receptors, Transforming Growth Factor beta
  • ginsenoside Rh2