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Cell invasion allows cells to migrate across compartment boundaries formed by basement membranes. Aberrant cell invasion is a first step during the formation of metastases by malignant cancer cells. Anchor cell (AC) invasion in  C .  elegans  is an excellent  in vivo  model to study the regulation of cell invasion during development. Here, we have examined the function of  egl-43 , the homolog of the human  Evi1  proto-oncogene (also called  MECOM ), in the invading AC.  egl-43  plays a dual role in this process, firstly by imposing a G1 cell cycle arrest to prevent AC proliferation, and secondly, by activating pro-invasive gene expression. We have identified the AP-1 transcription factor  fos-1  and the  Notch  homolog  lin-12  as critical  egl-43  targets. A positive feedback loop between  fos-1  and  egl-43  induces pro-invasive gene expression in the AC, while repression of  lin-12 Notch  expression by  egl-43  ensures the G1 cell cycle arrest necessary for invasion. Reducing  lin-12  levels in  egl-43  depleted animals restored the G1 arrest, while hyperactivation of  lin-12  signaling in the differentiated AC was sufficient to induce proliferation. Taken together, our data have identified  egl-43 Evi1  as an important factor coordinating cell invasion with cell cycle arrest.

plos genetics

The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion