c-Myc/BMI1 axis is essential for SETDB1-mediated breast tumorigenesis

Copy number gain/amplification of SETDB1 has been found in several human cancers, but the detailed oncogenic mechanism(s) of SETDB1 contributing to breast cancer remains largely unexplored. In this project, we analyzed the transcriptome of human breast cancer cell lines (MDA-MB-231 and MDA-MB-453) upon silencing of SETDB1 to explore the potential mechanism(s) underlying SETDB1 promoted breast cancer. In MDA-MB-231 cells, SETDB1 was silenced by shRNA-1. In MDA-MB-453 cells, SETDB1 was reduced by shRNA-3. Differences in gene expression was analyzed in breast cancer cell lines followed by shRNA mediated knock down of SETDB1