A mechanism explaining how epidermal growth factor (EGF) regulates breast cancer cell invasion is published online in Nature Cell Biology. The findings could contribute to the development of more specific anti-cancer drugs.
Highly proliferating, invasive breast cancer cells often express abnormally high levels of the EGF receptor (EGFR), and this is known to control both cell division and migration. In an effort to clarify the molecular pathways that are activated by EGFR specifically during cancer cell invasion -- as opposed to normal cell migration -- Hisataka Sabe and colleagues identify the protein GEP100 as a factor that directly links activated EGFR to Arf6, a protein that is often over expressed in breast cancer cells and promotes cancer cell invasion.
At high levels of GEP100, (as found in cancer cells), Arf6 was activated, allowing non-invasive cells to become invasive with stimulation of EGFR; conversely, when GEP100 was inhibited, metastasis was prevented in mice that had been injected with highly invasive breast cancer cells. Levels of GEP100 were enriched in clinical samples taken from invasive breast carcinomas, and the presence of GEP100 and EGFR correlated with tumour malignancy.
Inhibition of EGFR is an important anti-cancer treatment, although EGF also controls the growth of many normal cells. Thus, these findings could contribute to the development of more specific anti-cancer drugs that, by targeting GEP100, could efficiently block the pro-invasive activity of EGFR and inhibit the metastatic process.
Hisataka Sabe (Osaka Bioscience Institute, Japan)
Abstract available online.
(C) Nature Cell Biology press release.
Message posted by: Trevor M. D'Souza
Bookmark and Share this page (what is this?)
Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.
Use the links below to share this article on the social bookmarking site of your choice.
Read more about social bookmarking at Wikipedia - Social Bookmarking