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Mitogenic effects of oestrogen mediated by a non-genomic receptor in human colon

D C Winter1, C Taylor, G C O'Sullivan

  • 1Cork Cancer Research Centre and Department of Surgery, Mercy Hospital and Cellular Physiology Research Unit, University College Cork, Cork, Ireland.

The British Journal of Surgery
|December 21, 2000
PubMed
Abstract

Insights

Oestrogen rapidly increases cell proliferation in colorectal cancer via non-genomic pathways. This involves quick changes in cell membrane activity and intracellular pH, mediated by protein kinase C (PKC).

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cancer Research

Background:

  • Oestrogens act as mitogens in epithelial cancers, particularly those with oestrogen receptors.
  • Beyond traditional genomic pathways, rapid non-genomic actions of steroid hormones are recognized.
  • This study explores oestrogen's rapid effects on cell membrane, intracellular pH, and nuclear kinetics.

Purpose of the Study:

  • To investigate the hypothesis that oestrogen rapidly alters cell membrane activity, intracellular pH, and nuclear kinetics in a mitogenic manner.
  • To elucidate the mechanism of rapid oestrogen action in colorectal cancer cells.

Main Methods:

  • Utilized human distal colon crypts and colorectal cancer cell lines.
  • Measured DNA replication via thymidine incorporation and intracellular pH using spectrofluorescence imaging.
  • Inhibited genomic protein synthesis (cycloheximide), sodium-hydrogen exchanger (NHE) (ethylisopropylamiloride), and protein kinase C (PKC) (chelerythrine chloride).

Main Results:

  • Oestrogen induced rapid cellular alkalinization (<5 min) sensitive to NHE and PKC inhibition (P < 0.01).
  • Oestrogen significantly increased thymidine incorporation by 44% in crypts and up to 38% in cancer cells (P < 0.01).
  • This proliferative effect was reduced by inhibiting NHE (P < 0.01) or PKC (P < 0.05).

Conclusions:

  • Oestrogen rapidly activates cell membrane and nuclear kinetics through a non-genomic mechanism.
  • Protein kinase C (PKC) mediates this rapid, non-genomic oestrogen action.
  • Gene-directed protein synthesis is not required for these rapid oestrogen-induced effects.

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