Oestrogen causes G2/M arrest and apoptosis in breast cancer cells MDA-MB-231

Satoshi Nomoto, Yukitomo Arao, Hyogo Horiguchi, Kazuhiro Ikeda, Fujio Kayama

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

Flavonoids have been shown to exert many biological activities within cancer cells, and oestrogen is known to be structurally related to flavonoids. We investigated the effects of oestrogen in cancer cells to determine if its activities would be similar to those of flavonoids. When 50 μM 17β-oestradiol (oestradiol) was added to the oestrogen receptor (ER) α-negative breast cancer cell line MDA-MB-231, growth arrest was apparent, similar to that observed with genistein and daidzein. Oestradiol exhibited a dose response curve for the growth arrest similar to those of genistein and daidzein. Apoptosis occurred in the breast cancer cells after treatment with 50 μM oestradiol, genistein, or daidzein, with similar profiles. Flow cytometry analysis revealed that oestradiol treatment caused G2/M arrest and apoptosis. Cell-cycle arrest at G2/M began at 6 h after treatment, and apoptosis began within 24 h. Because MDA-MB-231 cells are ERα negative, these results suggest that oestradiol induces cell-cycle arrest and apoptosis through an ERα-independent pathway.

Original languageEnglish
Pages (from-to)773-776
Number of pages4
JournalOncology reports
Volume9
Issue number4
DOIs
Publication statusPublished - Jul 2002

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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