2-Methoxyestradiol induces G2/M arrest and apoptosis in prostate cancer

Laila R. Qadan, Carlos M. Perez-Stable, Curtis Anderson, Gianluca D'Ippolito, Alan Herron, Guy A. Howard, Bernard A. Roos

Research output: Contribution to journalArticlepeer-review

97 Scopus citations


Few therapeutic treatment options are available for patients suffering from metastatic androgen-independent prostate cancer. We investigated the ability of the estrogen metabolite 2-methoxyestradiol to inhibit the proliferation of a variety of human prostate cancer cell lines in vitro and to inhibit the growth of androgen-independent prostate cancer in a transgenic mouse model in vivo. Our results showed that 2-methoxyestradiol is a powerful growth inhibitor of LNCaP, DU 145, PC-3, and ALVA-31 prostate cancer cells. Cell flow cytometry of 2-methoxyestradiol-treated DU 145 cells showed a marked accumulation of cells in the G2/M phase of the cell cycle and an increase in the sub-G1 fraction (apoptotic). In addition, staining for annexin V, changes in nuclear morphology, and inhibition of caspase activity support a role for apoptosis. More importantly, we showed that 2-methoxyestradiol inhibits prostate tumor progression in the Gγ/T-15 transgenic mouse model of androgen-independent prostate cancer without toxic side effects. These results in cell culture and an animal model support investigations into the clinical use of 2-methoxyestradiol in patients with androgen-independent prostate cancer.

Original languageEnglish (US)
Pages (from-to)1259-1266
Number of pages8
JournalBiochemical and biophysical research communications
Issue number5
StatePublished - 2001


  • Annexins
  • Estrogens
  • Flow cytometry
  • Necrosis
  • Transgenic mice

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


Dive into the research topics of '2-Methoxyestradiol induces G2/M arrest and apoptosis in prostate cancer'. Together they form a unique fingerprint.

Cite this