Project description:We thoroughly analyzed the molecular subtyping of Triple-Negative Breast Cancer and its different manifestations, and located T cells and Tumor cells related to the survival of breast cancer through single cell sequencing and space transcriptome according to our score, and finally investigated their relationship with the therapeutic efficacy, providing a scientific basis for the treatment of triple negative breast cancer.
Project description:We thoroughly analyzed the molecular subtyping of Triple-Negative Breast Cancer and its different manifestations, and located T cells and Tumor cells related to the survival of breast cancer through single cell sequencing and space transcriptome according to our score, and finally investigated their relationship with the therapeutic efficacy, providing a scientific basis for the treatment of triple negative breast cancer.
Project description:Systems modelling of the EGFR-PYK2-c-Met interaction network predicted and prioritized synergistic drug combinations for Triple-negative breast cancer
Project description:We have utilized ChIPseq to identify the ER-beta cistrome in ER-beta expressing MDA-MB-231 triple negative breast cancer cells. ER-beta has been identified as a tumor suppressor in breast cancer and recent reports have demonstrated that ER-beta protein is detectable at moderate to high levels in approximately 30% of triple negative breast tumors. Increased expression of ER-beta in triple negative breast cancer has also been reported to be associated with improved recurrence-free survival. Treatment of ER-beta expressing triple negative breast cancer cells with estrogen, or the ER-beta selective agonist, LY500307, results in decreased cell proliferation, invasion and migration. To begin to identify the molecular mechanisms by which ER-beta elicits tumor suppressive effects in triple negative breast cancer, we performed ChIPseq studies and identified the genome-wide binding sites for ER-beta following exposure to 1nM estrogen or 10nM LY500307 for 3 hours. Over 28,000 and 10,000 unique ER-beta binding sites were identifed in response to these two ligands respectively. The top transcription factor motifs identified under both treatment conditions were estrogen response elements and AP1 response elements. The majority of ER-beta binding sites were found at enhancer regions located within introns or intergenic chromatin regions followed by gene promoters.
Project description:NUP93 expression inversely correlates with the survival of triple negative breast cancer patients. However, the role of NUP93 in tumor propagation has not yet been fully clarified. In this project we combined high-resolution imaging, migration assays and genetic analyses to demonstrate that NUP93 modulates actin cytoskeleton remodeling, epithelial-to-mesenchymal transition and invasion of triple negative breast cancer cells through direct interaction with the genome.
Project description:In the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al., we used NG Capture-C approach to identify regulatory elements interacting with the promoters of 35 Fra-1 regulated genes in the triple negative breast cancer cell line MDA-MB-231
