Project description:ATAC-seq profiling of luminal epithelial cells obtained from reduction mammoplasty tissue from young (<30 year) and old (>55 year) individuals.
Project description:The following data comes from two separate experiments. In the initial experiment, luminal and basal murine mammary epithelial cells were analyzed by reduced representation bisulfite sequencing (RRBS) to generate methylome profiles. In the second experiment, luminal and basal murine mammary epithelial cells were analyzed by ATAC-seq.
Project description:Global proteomic profiling of three mammary epithelial cell types in normal human breast tissue. Primary breast specimens were obtained from 10 women undergoing reduction mammoplasties. Clinical co-variates include age (28-67), hormone status (follicular, luteal, post-menopausal) and mammary epithelial cell type (basal, luminal progenitor, mature luminal).
Project description:Aging is one of the pivotal risk factors for cancer, notably in breast cancer with diagnosis striking at the average age of 62. However, the intricate mechanisms underlying aging and breast cancer susceptibility remain unclear. In this study, we depicted a comprehensive single-cell landscape of gene expression (scRNA-seq) and chromatin accessibility (scATAC-seq) of mammary glands from different aged rats. Mechanically, we revealed midkine, a growth factor secreted by basal epithelial cells, which might mediates the age-related mammary changes, as a validation, we treated young rats with midkine for a month and performed the single-cell transcriptome analysis on those mammary glands. We found midkine could largely mediates the transcriptional shift and hyperproliferation of aged epithelial cell by activating PI3K/AKT-SREBF1 signaling. Furthermore, we find the aging-related accumulation of midkine could largely mediated aging-related changes of mammary gland and promoting the tumorigenesis of breast tumors proved using a well-established Nitroso-N-methylurea (NMU)-induced breast cancer rat model. Our finding identify a promising biomarker and intervention target for both mammary aging and tumorigenesis.
Project description:Aging is one of the pivotal risk factors for cancer, notably in breast cancer with diagnosis striking at the average age of 62. However, the intricate mechanisms underlying aging and breast cancer susceptibility remain unclear. In this study, we depicted a comprehensive single-cell landscape of gene expression (scRNA-seq) and chromatin accessibility (scATAC-seq) of mammary glands from different aged rats. Mechanically, we revealed midkine, a growth factor secreted by basal epithelial cells, which might mediates the age-related mammary changes, as a validation, we treated young rats with midkine for a month and performed the single-cell transcriptome analysis on those mammary glands. We found midkine could largely mediates the transcriptional shift and hyperproliferation of aged epithelial cell by activating PI3K/AKT-SREBF1 signaling. Furthermore, we find the aging-related accumulation of midkine could largely mediated aging-related changes of mammary gland and promoting the tumorigenesis of breast tumors proved using a well-established Nitroso-N-methylurea (NMU)-induced breast cancer rat model. Our finding identify a promising biomarker and intervention target for both mammary aging and tumorigenesis.
Project description:Aging is one of the pivotal risk factors for cancer, notably in breast cancer with diagnosis striking at the average age of 62. However, the intricate mechanisms underlying aging and breast cancer susceptibility remain unclear. In this study, we depicted a comprehensive single-cell landscape of gene expression (scRNA-seq) and chromatin accessibility (scATAC-seq) of mammary glands from different aged rats. Mechanically, we revealed midkine, a growth factor secreted by basal epithelial cells, which might mediates the age-related mammary changes, as a validation, we treated young rats with midkine for a month and performed the single-cell transcriptome analysis on those mammary glands. We found midkine could largely mediates the transcriptional shift and hyperproliferation of aged epithelial cell by activating PI3K/AKT-SREBF1 signaling. Furthermore, we find the aging-related accumulation of midkine could largely mediated aging-related changes of mammary gland and promoting the tumorigenesis of breast tumors proved using a well-established Nitroso-N-methylurea (NMU)-induced breast cancer rat model. Our finding identify a promising biomarker and intervention target for both mammary aging and tumorigenesis.
Project description:The aim of this project is to examine age-dependent changes in the proteomes and phosphoproteomes of normal human mammary luminal epithelial and myoepithelial cells.