Project description:SMARCA4 loss-of-function induces cisplatin resistance to activate YAP1-dependent epithelial-to-mesenchymal in triple negative breast cancer
Project description:We report transcriptome profiling (RNA-seq) for SMARA4 knock-out to elucidate the association with cisplatin-resistance and SMARCA4 loss-of-function using triple negative breast cancer cell lines.
Project description:We report the genetic similarity of epithelial and mesenchymal subpopulations isolated from a triple-negative breast cancer cell line.
Project description:We report the chromatin accessibility of epithelial and mesenchymal subpopulations isolated from a triple-negative breast cancer cell line.
Project description:We characterize gene expression in epithelial and mesenchymal subpopulations isolated from a triple-negative breast cancer cell line in response to trametinib treatment.
Project description:We characterize histone modifications and transcription factor binding by ChIP-seq in epithelial and mesenchymal subpopulations isolated from a triple-negative breast cancer cell line.
Project description:We find that treating mesenchymal NAMEC8 cells with cholera toxin (CTx) to elevate intracellular cAMP levels and activate PKA induces a mesenchymal-to-epithelial transition whereby the cells assume an epithelial state (N8-CTx). NAMEC8 cells undergo epigenetic reprogramming triggered by active PHF2, a histone demethylase, which demethylates H3K9me2 and H3K9me3 regions of epithelial genes silencing in the mesenchymal state
Project description:We find that treating mesenchymal NAMEC8 cells with cholera toxin (CTx) to elevate intracellular cAMP levels and activate PKA induces a mesenchymal-to-epithelial transition whereby the cells assume an epithelial state (N8-CTx). NAMEC8 cells undergo epigenetic reprogramming triggered by active PHF2, a histone demethylase, which demethylates H3K9me2 and H3K9me3 regions of epithelial genes silencing in the mesenchymal state
Project description:Claudin-low breast cancer represents an aggressive molecular subtype that is comprised of mostly triple-negative mammary tumor cells that possess stem cell-like and mesenchymal features. Little is known about the cellular origin and oncogenic drivers that promote claudin-low breast cancer. In this study, we show that persistent oncogenic RAS signaling causes highly metastatic triple-negative mammary tumors in mice. More importantly, the activation of endogenous mutant KRAS and expression of exogenous KRAS specifically in luminal epithelial cells in a continuous and differentiation stage-independent manner induces preneoplastic lesions that evolve into basal-like and claudin-low mammary cancers. Further investigations demonstrate that the continuous signaling of oncogenic RAS as well as regulators of EMT play a crucial role in the cellular plasticity and maintenance of the mesenchymal and stem cell characteristics of claudin-low mammary cancer cells.
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.
