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Cdc42 regulates Cdc42EP3 function in Cancer-Associated FibroblastsCdc42 regulates Cdc42EP3 function in Cancer-Associated FibroblastsFarrugia AJ and Calvo F* 2017-01-01T23:00:00Z<p style="text-align:justify;"><span class="ms-rteThemeForeColor-2-5 ms-rteThemeFontFace-1 ms-rteFontSize-2">​<span style="font-weight:bold;">Abstract</span></span></p><div style="color:#000000;font-family:arial, helvetica, clean, sans-serif;text-align:justify;"><p style="margin-bottom:0.5em;font-size:1.04em;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">Rho family GTPases such as Cdc42 are key regulators of essential cellular processes through their effects on cytoskeletal dynamics, signaling and gene expression. Rho GTPases modulate these functions by engaging a wide variety of downstream effectors. Among these effectors is the largely understudied Cdc42EP/BORG family of Cdc42 effectors. BORG proteins have been linked to actin and septin regulation, but their role in development and disease is only starting to emerge. Recently, Cdc42EP3/BORG2 was shown to coordinate actin and septin cytoskeleton rearrangements in cancer-associated fibroblasts (CAFs). Interestingly, Cdc42EP3 expression potentiated cellular responses to mechanical stimulation leading to signaling and transcriptional adaptations required for the emergence of a fully activated CAF phenotype. These findings uncover a novel role for the BORG/septin network in cancer. Here, we demonstrate that Cdc42EP3 function in CAFs relies on tight regulation by Cdc42.</span><br></p></div><p><a href="">​Small GTPases Jan 2;8(1):49-57. </a><br></p>182