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The interplay between SOX4 and SMAD3 in the context of breast cancer

ABSTRACT: The interplay between SOX4 and SMAD3 in the context of breast cancer

PROVIDER: PRJNA413775 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6153880.fastq.gz	Fastqsanger.gz
	SRR6153890.fastq.gz	Fastqsanger.gz
	SRR6153900.fastq.gz	Fastqsanger.gz
	SRR6153920.fastq.gz	Fastqsanger.gz
	SRR6153930.fastq.gz	Fastqsanger.gz

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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.

2018-06-11 | GSE104760 | GEO

The interplay between SOX4 and SMAD3 in the context of breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below. The experiments are described in 2 papers: PMID 30137431 and PMID 30507376

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SMAD3 and SOX4 binding profiling in human breast cell lines

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Expression data for T24 bladder cancer cell line - scrambled, SOX4-KD and SOX4 overexpression

Project description:We knocked down SOX4 in T24 cell and created 3 cell lines: T24-scrambled, T24-SOX4-knockdown and T24-SOX4-rescue and compared gene expression changes SOX4 is a developmental transcription factor that is overexpressed in as many as 23% of bladder cancer patients, but the role of SOX4 in bladder cancer tumorigenesis is not well understood. Given SOX4’s many roles in embryonic development and context-dependent regulation of gene expression, we sought to understand SOX4’s contribution to bladder cancer and to elucidate SOX4 regulated genes that might contribute to tumorigenesis. We employed a CRISPR interference (CRISPRi) method to transcriptionally repress SOX4 expression in T24 bladder cancer cell lines, rescued these cell lines with lentivirally expressed SOX4, and performed whole genome expression profiling. SOX4 knockdown cells exhibited decreased invasive capabilities but no changes in migration or proliferation, while rescue with SOX4 lentiviral vector restored the invasive phenotype. Gene expression profiling revealed 173 high confidence SOX4 regulated genes

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SOX4 AND SMARCA4 COOPERATIVELY REGULATE PI3K SIGNALING THROUGH TRANSCRIPTIONAL ACTIVATION OF TGFBR2 IN TRIPLE NEGATIVE BREAST CANCER

Project description:Dysregulation of PI3K/Akt signaling is a dominant feature in basal-like or triple-negative breast cancers (TNBC). However, the mechanisms regulating this pathway are largely unknown in this subset of aggressive tumors. Here we demonstrate that the transcription factor SOX4 is a key regulator of PI3K signaling in TNBC. Genomic and proteomic analyses coupled with mechanistic studies identified TGFBR2 as a direct transcriptional target of SOX4 and demonstrated that TGFBR2 is required to mediate SOX4-dependent PI3K signaling. We further report that SOX4 and the SWI/SNF ATPase SMARCA4, which are uniformly overexpressed in basal-like tumors, form a previously unreported complex that is required to maintain an open chromatin conformation at the TGFBR2 regulatory regions in order to mediate TGFBR2 expression and PI3K signaling. Collectively, our findings delineate the mechanism by which SOX4 and SMARCA4 cooperatively regulate PI3K/Akt signaling and suggest that this complex may play an essential role in TNBC genesis and/or progression. Kinase enrichment proteomic analysis was performed using HCC1143 breast cancer cells treated with a control siRNA pool or a pool targeting SOX4 in biological triplicate to evaluate the effects on the functional kinome.

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SOX4 AND SMARCA4 COOPERATIVELY REGULATE PI3K SIGNALING THROUGH TRANSCRIPTIONAL ACTIVATION OF TGFBR2 IN BASAL LIKE BREAST CANCER

2021-03-02 | PXD022811 | Pride

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Project description:Analysis of the effect of shRNA-mediated knockdown of SOX4 on global gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of overlapping up- and downregulated genes in TRPM7 + SOX4 shRNA MDA-MB-231 cells

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Genome wide binding sites of Smad3 and JMJD3 in neural stem cells

Project description:Neural development requires crosstalk between signaling pathways and chromatin. In this study, we demonstrate that neurogenesis is promoted by an interplay between the TGFM-NM-2 pathway and the H3K27me3 histone demethylase (HDM) JMJD3. Genome-wide analysis showed that JMJD3 is targeted to gene promoters by Smad3 in neural stem cells (NSCs) and is essential to activate TGFM-NM-2-responsive genes. In vivo experiments in chick spinal cord revealed that the generation of neurons promoted by Smad3 is dependent on JMJD3 HDM activity. Overall, these findings indicate that JMJD3 function is required for the TGFM-NM-2 developmental program to proceed. We immunoprecipitate endogenous Smad3 or JMJD3 proteins from neural stem cells treated with TGFb for 30 minutes.

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Smad3 ChIP-chip analysis on human breast epithelial cells of the MCF10A series

Project description:TGF-betas have complex roles in tumorigenesis, with context-dependent effects that can either suppress or promote tumor progression. Our goal was to use integrated genomic approaches in a model of human breast cancer progression to identify core TGF-beta-regulated genes that specifically reflect the tumor suppressor activity of TGF-beta. The model consisted of the non-tumorigenic MCF10A (“M1”), the premalignant MCF10AT1k.cl2 (“M2”), the early malignant MCF10Ca1h (“M3”) and the highly malignant, metastatic MCF10Ca1a.cl1 (“M4”) cell lines. We have previously shown that tumor suppressor activity of TGF-beta is dependent on Smad3, and is lost in M4 cells. To identify how TGF-beta/Smad3 targets change with cancer progression, we performed promoter-wide Smad3 ChIP-chip on all four cell lines of the breast cancer progression model (M1-M4), following treatment with TGF-beta or vehicle control.

2015-01-01 | GSE34271 | GEO

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.

2020-01-01 | GSE99256 | GEO

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