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Learn MoreTo systemically study the molecular function of CARMIL3 in cancer cells, we used mammary tumor cells, 4T1, as a model and genetically depleted Carmil3 via CRISPR/Cas9 strategy, followed by genome-wide transcriptional analysis by RNA-seq. We find that loss of Carmil3 leads to down regulation of genes that are involved in cell adhesion, including Cdh1 which encodes E-cadherin, a marker of epithelial cells. Thus, our study suggests that CARMIL3 is implicated in regulating epithelial to mesenchymal transition and cancer metastasis. SOURCE: Xiaojing Ma Shanghai Jiao Tong University
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