Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA125887 | ENA |
REPOSITORIES: ENA
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Project description:This study was designed to identify genes that are differentially expressed when BP1 homeobox gene is overexpressed in MCF-7 breast cancer cells. The goal is to understand the functional role of BP1 in breast tumorigenesis. MCF-7 overexpressing pcDNA3.2-BP1 clones, O1 and O4 as replicates vs. MCF-7 transfected with pcDNA3.2 vector clones, V1 and V2 as replicates
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Project description:This study was designed to identify genes that are differentially expressed when BP1 homeobox gene is overexpressed in MCF-7 breast cancer cells. The goal is to understand the functional role of BP1 in breast tumorigenesis.
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Project description:<p>BRCA1 mutations are a hallmark of hereditary ovarian cancer, strongly linked to deficiencies in homologous recombination (HR) DNA repair and impaired DNA replication fork protection. However, its roles in cancer progression beyond maintaining genomic integrity remain poorly understood. Through metabolomics approaches, we found BRCA1-deficiency strikingly increased choline metabolism. Loss of BRCA1 promotes choline uptake through upregulating choline transporter-like protein 4 (CTL4). BRCA1 directly binds and recruits EZH2-mediated H3K27Me3 deposition to CTL4 promoter. CTL4 was therefore overexpressed in ovarian cancer tissues with BRCA1 mutations. Furthermore, BRCA1-deficiency significantly promotes ovarian cancer invasion, while inhibition of CTL4 reverses the high metastatic potential of BRCA1-deficient ovarian cancer cells, suggesting the functionality and specificity of CTL4 as a therapeutic target. Additionally, we discovered that phosphocholine, the choline metabolite increased by CTL4 overexpression, interacted with and stabilized the epithelial-to-mesenchymal transition inducer FAM3C in BRCA1-deficient ovarian cancer cells. Importantly, we identified a potent CTL4 inhibitor, DT-13, which significantly reduces choline metabolism and effectively suppresses metastasis in BRCA1-deficient ovarian cancers. Therefore, our study uncovers a mechanism underlying metastasis in BRCA1-deficient cancers and identifies CTL4 as a therapeutic target for metastatic ovarian cancer patients with BRCA1 mutations.</p>
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