The effects on the deficient of PRMT1 on gene expression for the acquisition of chemoresistance in triple negative breast cancer cells.
In cancer cells, metabolic programming is regulated by gene expression and/or by post-translational modifications of metabolic enzymes. The correlation between metabolic characteristics of breast cancer and their drug sensitivity has attracted much attention. Here, we investigated whether PRMT1, a major arginine methyltransferase, affects the expression levels of metabolic enzymes by mRNA expression profiling of wild-type and PRMT1 knockout cells of the breast cancer cell line MDA-MB-468 cells. The results strongly suggest that PRMT1-mediated breast cancer drug sensitivity is regulated by post-transcriptional rather than transcriptional regulation. Overall design: To investigate the function of PRMT1 for metabolic remodeling, we established PRMT1-knocking out cells in breast cancer cell line, MDA-MB-468.