What is it about?
For the first time, this article explains how active tumour cell division versus invasion, which are generally mutually exclusive events, may be regulated. In my previous articles I outline mechanisms through which MYB drives the growth of colon and breast cancers. In this article I demonstrate that MYB and its activity on cell division is inhibited by ZEB1, a gene which is turned on when breast cancer cells spread and squeeze themselves into nearby blood vessels. They achieve this via a cellular change termed Epithelial to Mesenchymal Transition, which is orchestrated by ZEB1 and other genes which act similar to ZEB1 to inhibit E-cadherin (read my reviews on this!).
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Why is it important?
Tumour cells that switch off their cell division and become invasive, via EMT, are harder to treat. Most traditional chemotherapies are aimed at shutting down the cell cycle. Cells that undergo EMT go "under the radar" and lie dormant in the body (cancer remission) then re-activate their cell division program resulting in "cancer relapse". If we can manipulate the cancer cell to remain in the actively proliferating (cell division), then traditional chemotherapies will be more effective.
Perspectives
This article formed a bridge between my PhD thesis work, focussing on mechanisms regulating the transcription of MYB in colon cancer, and my developing record in breast cancer EMT. This was my first major primary article publication in a high ranking journal and was supported by an NBCF Postdoctoral Training Fellowship.
Dr Honor J Hugo
Queensland University of Technology
Read the Original
This page is a summary of: Direct repression of MYB by ZEB1 suppresses proliferation and epithelial gene expression during epithelial-to-mesenchymal transition of breast cancer cells, Breast Cancer Research, January 2013, Springer Science + Business Media,
DOI: 10.1186/bcr3580.
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