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