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BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [ChIP-Seq]

ABSTRACT: BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [ChIP-Seq]

PROVIDER: PRJNA511964 | ENA |

REPOSITORIES: ENA

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BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer

Project description:BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer

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BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [RNA-seq]

Project description:BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [RNA-seq]

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BACH1 alters the expression of EMT-related genes to promote metastasis in pancreatic cancer [RNA-seq]

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.

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Investigating a Novel Interaction of c-MET and BACH1 in Head and Neck Squamous Cell Carcinoma Metastasis

Project description:Metastasis is estimated to be responsible for 90% of cancer deaths, and fewer than 10% of patients with metastatic head and neck squamous cell carcinoma (HNSCC) survive beyond 5 years. HNSCC is responsible for upwards of 270,000 global deaths annually, with up to 30% more cases projected annually by 2030. The proto-oncogene MET encodes for the tyrosine kinase receptor c-MET, which is overexpressed in over 80% of human papilloma virus (HPV)-negative HNSCC cases and particularly enriched in metastatic lymph nodes. c-MET is activated by its ligand, hepatocellular growth factor (HGF), and is known to promote cancer cell migration, proliferation, and metastasis through a variety of downstream effectors. Thus far, unfortunately, inhibition of c-MET has shown low efficacy as a single-agent therapy in clinical trials, which indicates a need for further understanding of the mechanisms underlying c-MET-mediated metastasis in HNSCC. We show here that human HNSCC cells upregulate expression of the transcription factor BACH1 through c-MET activation upon HGF treatment. In accordance with previous reports, HGF activation increased expression of epithelial-mesenchymal transition (EMT) markers. Similarly, BACH1 suppression reduced expression of these EMT markers. By pharmacological inhibition of c-MET by FDA-approved capmatinib in combination with hemin treatment to reduce BACH1 expression, migration was reduced compared to either treatment alone in scratch-wound migration assays. Collectively, these data indicate that BACH1 and c-MET are both necessary for the regulation of EMT and migration in HNSCC. Our data suggest the potential for combination therapy targeting both c-MET and BACH1 to reduce HNSCC metastasis.

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The transcription repressors Bach2 and Bach1 promote B cell development by repressing the myeloid program

Project description:Mature lymphoid cells express the transcriptional repressor Bach2, which imposes regulation on humoral and cellular immunity. Here we found critical roles for Bach2 in the development of cells of the B lineage, commencing from the common lymphoid progenitor (CLP) stage, with Bach1 as an auxiliary. Overexpression of Bach2 in pre-pro-B cells deficient in the transcription factor EBF1 and single-cell analysis of CLPs revealed that Bach2 and Bach1 repressed the expression of genes important for myeloid cells (M-bM-^@M-^Xmyeloid genesM-bM-^@M-^Y). Bach2 and Bach1 bound to presumptive regulatory regions of the myeloid genes. Bach2hi CLPs showed resistance to myeloid differentiation even when cultured under myeloid conditions. Our results suggest that Bach2 functions with Bach1 and EBF1 to promote B cell development by repressing myeloid genes in CLPs. WT and Bach1 and Bach2 double deficient (DD) CLPs. Multipotent progenitors (MPPs) infected with control-GFP and Bach2-GFP and cultured several condition. Follicular B cells (Fo B) stimulated with IgM. Three expreriments was performed in this paper.

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