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Epigenetic Landscapes in Breast Cancer Cells

ABSTRACT: Chromatin architecture is essential to transcriptional regulation. Cancer cells undergo critical chromatin remodeling processes that interact with the activation or silencing of oncogenes or tumor suppressor genes. These processes, together with other alterations of the functional status of chromatins, are characterized by epigenetic marks such as covalent histone modifications, DNA methylations and etc. The epigenetic landscapes defined by these marks are key to understand their regulatory mechanisms as well as the contributions to cancer onset and progression. In this study, we focus on defining the epigenetics landscapes across different breast cancer subtypes. Here we present a collection of 11 key histone modifications across 13 distinct breast cancer cell lines, representing 5 major breast cancer subtypes, including two ER positive subtypes: Lumina-A and Lumina-B, HER2 positive subtype and triple-negative subtypes TNBC-Basal and TNBC-ClaudinLow, as well as normal-like immortal breast cells. Using combinatorial patterns of multiple histone modifications, we defined the whole genome chromatin state maps and identified specific signatures in breast cancer subtypes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE85158 | GEO | 2017/12/15

SECONDARY ACCESSION(S): PRJNA336352

REPOSITORIES: GEO

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Project description:Breast cancer is a heterogeneous disease for which prognosis and treatment strategies are largely governed by the receptor status (estrogen, progesterone and Her2-neu) of the tumor cells. Gene expression profiling of whole breast tumors further stratifies breast cancer into several molecular subtypes which also co-segregate with the receptor status of the tumor cells. We postulated that cancer associated fibroblasts (CAFs) within the tumor stroma may exhibit subtype specific gene expression profiles and thus contribute to the biology of the disease in a subtype specific manner. Several studies have reported gene expression profile differences between CAFs and normal breast fibroblasts but in none of these studies were the results stratified based on tumor subtypes. To address whether gene expression in breast cancer associated fibroblasts varies between breast cancer subtypes, we compared the gene expression profiles of early passage primary CAFs isolated from twenty human breast cancer samples representing three main subtypes; seven ER+, seven triple negative (TNBC) and six Her2+. We observed significant expression differences between CAFs derived from Her2+ breast cancer and CAFs from TNBC and ER+ cancers, particularly in pathways associated with cytoskeleton and integrin signaling. In the case of Her2+ breast cancer, the signaling pathways found to be selectively up regulated in CAFs may contribute to the more invasive properties and unfavorable prognosis of Her2+ breast cancer. These data demonstrate that in addition to the distinct molecular profiles that characterize the neoplastic cells, CAF gene expression is also differentially regulated in distinct subtypes of breast cancer. We isolated CAFs from twenty primary breast cancer samples representing three main subtypes (ER+ (n=7), TNBC (n=7), Her2+ (n=6)) and performed gene expression profile analyses on RNA isolated from these early passage CAFs. Those samples were done in two batches with 4 samples repeated in both batches. One TNBC sample was found to be an outlier and not used in the analysis.

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Epigenetic Landscapes in Breast Cancer Cells

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