Gene expression profiling of control and Carmil3-deficient 4T1 cells

To 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. Overall design: The mRNA expression profiles between control and Carmil3 KO 4T1 cells were compared with RNA-seq in triplicate.