Project description:Chronic stress triggers activation of the sympathetic nervous system (SNS) and drives malignancy. Using an immunodeficient murine system, we show that chronic stress promotes breast cancer stem-like properties via lactate dehydrogenase A (LDHA) dependent metabolic rewiring. In this dataset, we used microarray to characterize the mRNA expression profiles from primary PBS and Epinephrine -treated MDA-MB-231 tumor cells.
Project description:we investigated the effects of IH and epinephrine on gene expression in human aortic ECs using RNA-sequencing. We found a significant overlap between IH and epinephrine-induced differentially expressed genes (DEGs).
Project description:The importance of the impact of human hormones on commensal microbiota and microbial biofilms is established in lots of studies. In the present investigation, we studied the proteome of biofilms and planktonic cultures of skin actinobacterium Cutibacterium acnes. In our investigation, we tested the effect of epinephrine in concentrations 5 nM (normal blood level) and 5 µM (1000-fold higher) on 72 h biofilms and planktonic cultures in comparison with controls without the hormone administration. Also, we compared the samples treated with epinephrine in different concentrations. Also, we investigated the differences between planktonic cultures and biofilms and how the hormone influences those differences. The present database contains the raw data of proteins changes in their concentrations in described conditions.
Project description:To investigate the trancriptomic changes of tumor endothelial cells (ECs) in response to STING activation, tumor ECs from MMTV-PyMT mouse model or implanted breast tumour model were either treated by PBS or cGAMP were sorted by FACS and single-cell RNA seq was performed.
Project description:The importance of the impact of human hormones on commensal microbiota and microbial biofilms is established in lots of studies. In the present investigation, we studied the proteome of the biofilm matrix of the commensal actinobacterium Micrococcus luteus C01. In our investigation, we tested the effect of epinephrine in concentration 4.9×10-9 M on immature (24 h ) and mature (72 h) biofilms in comparison with controls without the hormone administration. We investigated the temporal changes in the matrix proteome during the incubation in control samples and in samples with epinephrine.
Project description:Male and female mice were injected with NaCl vs epinephrine to induce acute paradoxical reversible heart failure akin to Takotsubo Syndrome with subsequent RNASeq analysis of left ventricular tissue.
Project description:Therapeutic combinations to alter solid tumor microenvironments (TME) in immunosuppressive tumors such as breast cancer are essential to improve their responses to immune checkpoint inhibitors (ICIs). Entinostat, an oral histone deacetylase inhibitor (HDACi), has been shown to improve responses to ICIs in various tumor models with immunosuppressive TMEs. The precise and comprehensive alterations to the TME induced by entinostat remain unknown. Here, we employ single-cell RNA-sequencing on HER2 overexpressing breast tumors from mice treated with entinostat and ICIs to characterize for the first time changes across all cell types within the TME. This analysis demonstrates that treatment with entinostat induces a shift from a pro-tumor to an anti-tumor TME signature characterized predominantly by changes in the myeloid cells. We confirm myeloid-derived suppressor cells (MDSCs) within entinostat-treated tumors are associated with a less suppressive G-MDSC phenotype and now demonstrate altered suppressive signaling involves the NFkB and STAT3 pathways. In addition to MDSCs, tumor-associated macrophages are epigenetically reprogrammed toward an anti-tumor M1-like phenotype likely contributing to a more sensitized TME. Overall, our in-depth analysis suggests entinostat-induced changes on multiple myeloid cell types reduce immunosuppression and increase mechanisms of an anti-tumor response that improve sensitivity to ICI. Sensitization of the TME by entinostat could ultimately broaden the population of patients with breast cancer who could derive benefit from ICIs.