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The homeoprotein Six2 promotes breast cancer metastasis via transcriptional and epigenetic control of E-cadherin expression

ABSTRACT: Mouse mammary carcinoma cell line 4TO7 was used in this experiment. Six2 overepxression experiment.The mouse Six2 cDNA taken from CMV-sport6 (Open Biosystems) was cloned into a pcDNA3.1-hygromycin vector and transfected into 4TO7 cells, after which stably transfected cells were selected. Gene expression profiles were performed in triplicate for the control and over-expressed lines.

ORGANISM(S): Mus musculus

PROVIDER: GSE57678 | GEO | 2014/12/31

SECONDARY ACCESSION(S): PRJNA247776

REPOSITORIES: GEO

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Homeoprotein Six2 promotes breast cancer metastasis via transcriptional and epigenetic control of E-cadherin expression.

Project description:Misexpression of developmental transcription factors occurs often in human cancers, where embryonic programs may be reinstated in a context that promotes or sustains malignant development. In this study, we report the involvement of the kidney development transcription factor Six2 in the metastatic progression of human breast cancer. We found that Six2 promoted breast cancer metastasis by a novel mechanism involving both transcriptional and epigenetic regulation of E-cadherin. Downregulation of E-cadherin by Six2 was necessary for its ability to increase soft agar growth and in vivo metastasis in an immunocompetent mouse model of breast cancer. Mechanistic investigations showed that Six2 represses E-cadherin expression by upregulating Zeb2, in part, through a microRNA-mediated mechanism and by stimulating promoter methylation of the E-cadherin gene (Cdh1). Clinically, SIX2 expression correlated inversely with CDH1 expression in human breast cancer specimens, corroborating the disease relevance of their interaction. Our findings establish Six2 as a regulator of metastasis in human breast cancers and demonstrate an epigenetic function for SIX family transcription factors in metastatic progression through the regulation of E-cadherin.

| S-EPMC4268359 | biostudies-literature

Gene expression profiling of Six2-positive nephron progenitors from mouse embryo

Project description:Nephron progenitors in the embryonic kidney propagate while generating differentiated nephrons. However, the progenitors in mice terminally differentiate shortly after birth. We defined culture conditions to selectively propagated nephron progenitors in vitro in an undifferentiated state. To understand how expression profiles of Six2+ cells changed during culture in vitro compared with in vivo, we performed microarray analysis of Six2+ cells at E11.5 (starting material) and P0 (experiencing 8 days in vivo), and cultured Six2+ cells at E11.5 for 8 days or 19 days. Microarray analysis were performed with isolated Six2-positive nephron progenitors from transgenic mice embryo at E11.5 or P0, and cultured E11.5 Six2+ cells for 8 or 19 days in conditioned media. P0 non-progenitors represent Six2-GFP-negative cells at P0.

2016-04-14 | E-GEOD-79024 | biostudies-arrayexpress

Genome-wide maps of Six2 and b-catenin in mesenchymal nephron progenitors

Project description:Self-renewing undifferentiated nephron progenitors express Six2, a transcription factor that is required for their maintenance as undifferentiated progenitors. Differentiation of nephron progenitors is triggered by Wnt/b-catenin signaling. In order to understand how Six2 and Wnt signaling counteract each other, we performed ChIP-seq of Six2 and b-catenin in mesenchymal nephron progenitor cells. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. For Six2 ChIP, freshly FACS isolated Six2+ cells were used. For b-catenin ChIP, FACS isolated Six2+ cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing 4uM BIO for 24hrs.

2012-09-11 | E-GEOD-39837 | biostudies-arrayexpress

RNA-seq Analysis in 4T07 Control (4T07-CTL) and Six2 Overexpression (4T07-Six2) cells

Project description:To determine the molecular mechanisms by which Six2 regulates metastatic colonization, we performed RNA-seq analysis on murine triple-negative 4T07 Control (4T07-CTL) and Six2 overexpressing (4T07-Six2) cells. Using both targeted and unbiased gene signature analyses, we found that Six2 differentially regulates gene signatures associated with stemness. Additionally, we confirmed that in several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes (identified as among the highest upregulated genes in response to Six2 overexpression) associated with embryonic stem cell programs. When combined with our in vitro and in vivo stemness-associated phenotypic assays, these data suggest that Six2 may play a similar role in mediating stemness characteristics during tumor progression as it does during development, and that this role may allow it to mediate late-stage metastasis by enhancing the ability of cells to self-renew and survive at secondary sites.

2020-01-30 | GSE123489 | GEO

Exploring Six2 distal enhancer interactome in developing mouse kidney

Project description:The Six2 distal enhancer regulates expression of the 60 kb-downstream gene Six2, but does not regulate the Six3 gene which is 70 kb further downstream. CTCF ChIP-Seq and Hi-C data points to a chromatin domain boundary between Six2 and Six3 which may intervene interaction between Six2-DE and Six3. The irradiation-induced Brachyrrhine (Br) mutant allele was found to carry a 320 kb genomic inversion that includes Six2 and Six3, but not Six2DE. This repositioned Six2 under Six3 enhancer control and Six3 under Six2 distal enhancer control. Consistent with this, Six3 is ectopically expressed in Br/+ kidneys and Six2 expression is reduced. To test whether there is a change of interaction between Six2 distal enhancer and Six2 or Six3 promoters, we performed 4C-Seq in E16.5 wildtyp or Br/+ mice nephron-genic zone cells.

2018-01-18 | GSE108102 | GEO

Expression analysis of Human esophagus cancer cell line TE-1 transfected with PCDNA3.1 and PCDNA3.1-Pax2

Project description:Investigation of whole genome gene expression level changes of TE-1 transfected with PCDNA3.1-Pax2 ,compared to TE-1 transfected with PCDNA3.1.

2014-12-12 | GSE64093 | GEO

hPTTG1-/- HCT116 human colorectal cancer cells: pcDNA3.1 control vs. pcDNA3.1-hPTTG1

Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid.

2014-01-02 | GSE26434 | GEO

Transcriptional responses in SIX2 nephron progenitor cells following mitochondrial complex III subunit 7 (Qpc) inactivation

Project description:To identify novel transcriptional targets following Qpc inactivation. We deleteted Qpc in SIX2 nephron progenitor cells using a Six2-eGFP/cre BAC transgene. We compared SIX2-expressing progenitors from Six2-Qpc-/- kidneys with control (Six2-Qpc+/-) embryonic kidneys at E18.5.

2022-06-29 | GSE158299 | GEO

Overexpression of MXRA7 in murine prostate cancer cell line RM1

Project description:Murine prostate cancer cells RM1 were transfected with a fakery murine MXRA7 cDNA in pcDNA3.1 vector. Controls were RM1 transfected with pcDNA3.1 vector. G418 resistant colonies were obtained, and gene expression profiling was performed using Agilent 4*44K array and dual labeling.

2017-07-01 | GSE89543 | GEO

Huntingtin contains an ubiquitin-binding domain and regulates lysosomal targeting of mitochondrial and RNA-binding proteins

Project description:Evaluating the identity of ubiquitinated and ubiquitin-associated proteins tandem co-purifying non-covalently with wild-type (17 glutamine) human Huntingtin fragment, amino acids 1-502 C-terminally tagged with the HA peptide epitope, basally expressed from the CMV promoter within vector pcDNA3.1 transiently transfected into striatal precursor cell line St14A, significantly elevated above cells transfected with empty pcDNA3.1 vector negative control, in cells co-transfected with human FLAG-ubiquitin.

2024-07-31 | PXD053980 | Pride

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