TANK binding kinase 1 induces transcription factor BACH1 to regulate iron metabolism in pancreatic cancer cells

BTB and CNC homology 1 (BACH1) represses the expression of genes involved in the metabolism of iron, heme and reactive oxygen species and promotes metastasis of various cancers including pancreatic ductal adenocarcinoma (PDAC). Knockdown of Tank binding kinase 1 (TBK1) led to reductions of BACH1 mRNA and protein amounts in AsPC-1 human PDAC cells. Gene expression analysis of PDAC cells with knockdown of TBK1 or BACH1 suggested the involvement of TBK1 and BACH1 in the regulation of iron homeostasis. Ferritin was increased upon BACH1 knockdown in AsPC-1 cells. Cytometry analysis showed that AsPC-1 cells with BACH1 knockout or knockdown contained lower labile iron than control cells, suggesting that BACH1 increased labile iron by repressing the expression of ferritin genes. Overall design: RNA sequencing of total 4 samples was performed. Each sample is biologically duplicated. There are two different conditions: Total RNA of stealth RNA and negative control treatment against TBK1 in AsPC-1, the pancreatic cancer cell line.