Project description:Metastatic progression remains the major cause of death in human breast cancer. Cancer cells with cancer stem cell (CSC) properties drive initiation and growth of metastases at distant sites. We have previously established the breast cancer patient-derived tumor xenograft (PDX) mouse model in which CSC marker CD44+ cancer cells formed spontaneous microscopic metastases in the liver. In this PDX mouse, the expression levels of S100A10 and its family proteins were much higher in the CD44+ cancer cells metastasized to the liver than those at the primary site.
Project description:To investigate the properties of breast cancer stem cells, we generated sphere cells derived from adherent cells of breast cancer cell line, MCF-7, and obtained gene expression data of Illumina Gene Chip Arrays.
Project description:Breast cancer stem cells are considered estrogen receptor negative and estrogen insensitive. However, estrogens potentiate growth of the vast majority of breast tumors. In this study, we characterize the expression of estrogen receptors in breast cancer stem cells. We used microarrays to characterize the global gene expression underlying estrogen receptor activation versus inhibition in breast cancer cells from invasive breast cancers. Cancer cells from invasive breast carcinomas are treated with D (DPN), T (4OHT) or untreated (vehicle control).
Project description:Breast cancer stem cells are considered estrogen receptor negative and estrogen insensitive. However, estrogens potentiate growth of the vast majority of breast tumors. In this study, we characterize the expression of estrogen receptors in breast cancer stem cells. We used microarrays to characterize the global gene expression underlying estrogen receptor activation versus inhibition in breast cancer cells from invasive breast cancers.
Project description:Overcoming endocrine-resistance is the major challenge in treating Estrogen receptor (ER)-positive breast cancer. Breast Cancer Stem Cells (BCSCs) are blamed to be the driving force behind poor clinical outcomes and therapeutic resistance. Tumor microenvironment (TME) exerts a selective pressure on the tumor, supporting BCSCs behavior. The most prevalent cellular component of breast TME is represented by adipocytes, which secrete reduced levels of adiponectin in obesity, promoting ERα-positive breast cancer growth and progression. We examined the impact of low adiponectin levels on the enrichment of BCSC subpopulations and the molecular mechanisms by which this may contribute to hormone-resistance in breast cancer.