TY - JOUR AB - Despite critical roles in development and cancer, the mechanisms that specify invasive cellular behavior are poorly understood. Through a screen of transcription factors in Caenorhabditis elegans, we identified G1 cell-cycle arrest as a precisely regulated requirement of the anchor cell (AC) invasion program. We show that the nuclear receptor nhr-67/tlx directs the AC into G1 arrest in part through regulation of the cyclin-dependent kinase inhibitor cki-1. Loss of nhr-67 resulted in non-invasive, mitotic ACs that failed to express matrix metalloproteinases or actin regulators and lack invadopodia, F-actin-rich membrane protrusions that facilitate invasion. We further show that G1 arrest is necessary for the histone deacetylase HDA-1, a key regulator of differentiation, to promote pro-invasive gene expression and invadopodia formation. Together, these results suggest that invasive cell fate requires G1 arrest and that strategies targeting both G1-arrested and actively cycling cells may be needed to halt metastatic cancer. AU - Matus,DQ AU - Lohmer,LL AU - Kelley,LC AU - Schindler,AJ AU - Kohrman,AQ AU - Barkoulas,M AU - Zhang,W AU - Chi,Q AU - Sherwood,DR DO - 10.1016/j.devcel.2015.10.002 EP - 174 PY - 2015/// SN - 1534-5807 SP - 162 TI - Invasive cell fate requires G1 Cell-cycle arrest and histone deacetylase-mediated changes in gene expression T2 - Developmental Cell UR - http://dx.doi.org/10.1016/j.devcel.2015.10.002 UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000363868300004&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202 UR - https://www.sciencedirect.com/science/article/pii/S1534580715006292?via%3Dihub VL - 35 ER -