Project description:Macrophages are central in regulating iron homeostasis. Transcription repressor Bach1 regulates by heme. Here we investigated the relationship between heme-regulated Bach1 and bone marrow derived macrophage. We found that Bach1 KO macrophage showed that up-regulated genes were the process that iron-heme homeostasis and maintenance related gene compared with WT. Our results suggest that Bach1 expression is important to the heme homeostasis and maintenance in the bone marrow derived macrophage.
Project description:BTB and CNC homology 1 (BACH1) has been implicated in RAS-driven tumor formation. We focused on the role of BACH1 in Pancreatic ductal adenocarcinoma (PDAC), more than 90% of which have KRAS mutation. BACH1 directly or indirectly repressed the expression of genes for epithelial cell adhesion in AsPC-1 cells and SW1990. Knockdown and overexpression of BACH1 in PDAC cell lines indicated that BACH1 promoted cell migration and invasion in part by reducing E-cadherin expression.
Project description:BTB and CNC homology 1 (BACH1) has been implicated in RAS-driven tumor formation. We focused on the role of BACH1 in Pancreatic ductal adenocarcinoma (PDAC), more than 90% of which have KRAS mutation. BACH1 directly or indirectly repressed the expression of genes for epithelial cell adhesion in AsPC-1 cells and SW1990. Knockdown and overexpression of BACH1 in PDAC cell lines indicated that BACH1 promoted cell migration and invasion in part by reducing E-cadherin expression.
Project description:Since the primary effect of the ketogenic diet is to establish a glucose-deprived condition in vivo, we, therefore, used glucose starvation in vitro to mimic the effects of the keto diet. In our endeavor to comprehend the influence of glucose starvation on pro-metastatic genes associated with BACH1, we performed RNA-Seq analysis on MDA-MB-231 ctrl cells and BACH1 knockout cells.
Project description:The transcription factor BACH1 is a master regulator of human breast cancer metastasis. Here we use gene expression array analysis to identify and compare the genes regulated by BACH1 depletion in a metastatic human breast cancer cell line. Total RNAs were extracted from vector control 1833 cells or 1833 cells with shBACH mRNA BACH1 depletion. Affymetrix GeneChip Human Gene 1.0 ST Arrays were performed to detail the gene expression and identify the genes regulated by BACH1in metastatic human breast cancer cells.
Project description:Purpose: To gain futher insight into how microglia-derived BACH1 regulates microglial metabolism and astrogenesis, RNA-seq was used to analyze the genome-wide changes resulting from isolated microglia of E16 microglial BACH1 conditional knock out mice and littermate wild-type. Methods: mRNA from E16 isolated microglia of Bach1fl/fl and Bach1cKO-Cx3 mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately one thousand transcripts showed differential expression between the Bach1fl/fl and Bach1cKO-Cx3 mice brain microglia, with a fold change ≥3 and p value <0.05. Geneontology analysis of the downregulated genes were enriched in terms related to cell proliferation, glial cell differentiation and cell communication and upregulated genes were enriched in terms related to negative regulation of cell proliferation, negative regulation of astrocyte differentiation and glial cell fate commitment. These results reflected microglia BACH1 plays roles in cortex development. Conclusions: Microglia BACH1 RNA-seq would provide a overall understanding how microglia-derived BACH1regulates astrogenesis during brain development.
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.