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The effects of SOX4 on the global epigenetic landscape in Mammary Epithelial Cells

ABSTRACT: By chromatine-immunoprecipitating (ChIP) using the mammary epithelial cell line HMLE with a Doxycyclin-inducible overexpression of SOX4 we determined various histone modifications and presence of the POL2 polymerase in presence and absence of overexpressed SOX4.

ORGANISM(S): Homo sapiens

PROVIDER: GSE125643 | GEO | 2019/01/26

REPOSITORIES: GEO

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SMAD3 and SOX4 binding profiling in human breast cell lines

Project description:In order to identify genes co-bound by SOX4 and SMAD3 in the context of breast cancer, different breast cell lines (HMLEs, MDA-MB-231 or HCC-1954) were used. Due to low endogenous expression levels for SOX4 in HMLEs in untreated conditions, doxycycline-dependent SOX4 overexpression was obtained by transducing HMLE cells with pIINDUCER21-SOX4 vector..Cells were plated and SOX4 and SMAD3 chromatine-immunoprecipitation was performed in untreated conditions, TGF-beta (2.5ng/ml), doxycycline (0.5ug/ml) or both as indicated. Genome-wide binding sites for SOX4 and SMAD3 was identified in HMLEs, MAD-MB-231 and HCC-1954 cells.

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RNA-sequencing of mouse mammary tumor organoids that were modified to generate knockout lines for SOX4

Project description:The transcription factor SOX4 is widely expressed during development and is essential to maintain progenitor pools in a variety of organs. In breast cancer SOX4 has been shown to be associated with poor survival and increased tumor size and metastasis formation. This has mostly been attributed to the ability of SOX4 to regulate Epithelial-to-Mesenchymal-Transition (EMT). However, SOX4 regulates target gene transcription in a plastic manner that is dependent on the cellular and epigenetic context. In this study we have investigated the loss of SOX4 in mammary tumor development utilizing organoids derived from a PyMT genetic mouse model. CRISPR-mediated loss of SOX4 led to a strong impairment in growth of primary mammary tumors and subsequent metastases through an EMT-independent mechanism. Instead, SOX4 is required for inhibiting differentiation by controlling genes that are highly activated in foetal mammary stem cells (fMaSC). These SOX4-dependent genes are associated with cell cycle progression, DNA biosynthesis, RNA processing and ribosome biogenesis suggesting that SOX4 controls active cycling of tumor cells. Analysis of genes co-expressed with SOX4 in the TCGA and METABRIC studies revealed that these cell cycle-related genes correlate with SOX4 expression in human tumors. Our study identifies a novel role for SOX4 in maintaining mammary tumors in an undifferentiated proliferative state.

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Gene expression profiling of epithelial and mesenchymal subpopulations within immortalized human mammary epithelial cells

Project description:For gene expression profiling, we used immortalized human mammary epithelial cells (HMLE) to isolate a pure epithelial fraction of cells by positive selection for CD24 expression using Magnetic Activated Cell Sorting (=24hi). We independently isolated 3 mesenchymal subpopulations (msp1-3) from HMLE cells by collecting floating cells from cultured monolayer HMLE cells.

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Global transcriptional analysis identifies a novel role for SOX4 in tumor-induced angiogenesis

Project description:The expression of the transcription factor SOX4 is increased in many human cancers, however, the pro-oncogenic capacity of SOX4 can vary greatly depending on the tumor-type. Both the contextual nature and the mechanisms underlying the pro-oncogenic SOX4 response remain unexplored. Here, we demonstrate that in mammary tumorigenesis, the SOX4 transcriptional network is dictated by the epigenome and is enriched for pro-angiogenic processes. We show that SOX4 directly regulates endothelin-1 (ET-1) expression and thereby promotes tumor-induced angiogenesis both in vitro and in vivo. Furthermore, in breast tumors, SOX4 expression correlates with blood vessel density and size, and predicts poor-prognosis in breast cancer patients. Our data provide novel mechanistic insights into context-dependent SOX4 target gene selection, and uncover a novel pro-oncogenic role by promoting tumor-induced angiogenesis. These findings establish a key role for SOX4 in promoting metastasis through exploiting diverse pro-tumorigenic pathways.

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SOX4 facilitates PGR protein stability and FOXO1 expression conducive for human endometrial decidualization

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