Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA169317 | ENA |
REPOSITORIES: ENA
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Project description:Regulatory factors controlling stem cell identity and self-renewal are often active in aggressive cancers and are thought to promote their growth and progression. TCF3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic stem (ES) cell identity. We found that TCF3 is highly expressed in poorly differentiated human breast cancers, preferentially of the basal-like subtype. This suggested that TCF3 is involved in the regulation of breast cancer cell differentiation state and tumorigenicity. Silencing of TCF3 dramatically decreased the ability of breast cancer cells to initiate tumor formation, and led to decreased tumor growth rates. In culture, TCF3 promotes the sphere formation capacity of breast cancer cells and their self-renewal. We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells, while repressing another distinct target subset. In the normal mouse mammary gland Tcf3 is highly expressed in terminal end buds, structures that lead duct development. Primary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the developing gland disrupts ductal growth. Our results identify TCF3 as a central regulator of tumor growth and initiation, and a novel link between stem cells and cancer. Cells infected with different shRNA vectors were either untreated, treated with control or Wnt3A condition medium. Condition medium treatments were done in biological repeats.
2012-10-23 | E-GEOD-38893 | biostudies-arrayexpress
Project description:Regulatory factors controlling stem cell identity and self-renewal are often active in aggressive cancers and are thought to promote their growth and progression. TCF3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic stem (ES) cell identity. We found that TCF3 is highly expressed in poorly differentiated human breast cancers, preferentially of the basal-like subtype. This suggested that TCF3 is involved in the regulation of breast cancer cell differentiation state and tumorigenicity. Silencing of TCF3 dramatically decreased the ability of breast cancer cells to initiate tumor formation, and led to decreased tumor growth rates. In culture, TCF3 promotes the sphere formation capacity of breast cancer cells and their self-renewal. We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells, while repressing another distinct target subset. In the normal mouse mammary gland Tcf3 is highly expressed in terminal end buds, structures that lead duct development. Primary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the developing gland disrupts ductal growth. Our results identify TCF3 as a central regulator of tumor growth and initiation, and a novel link between stem cells and cancer.
2012-10-23 | GSE38893 | GEO
Project description:The mechanisms that allow breast cancer cells to metabolically sustain growth are poorly understood. In breast cancer, FoxA1 transcription factor, along with estrogen receptor, regulates luminal cell specification and proliferation. Here we report that FoxA transcription factor family members FoxA1 and FoxA2 fuel cellular growth in breast cancer through the expression of a common target gene, namely the endothelial lipase (LIPG) We used microarrays to detail the genes that are under de control of FoxA transcription factors in MDA231 and MCF7 breast cancer cells
2016-04-08 | GSE61164 | GEO
Project description:Breast cancer is the most common cancer in women worldwide and metastatic dissemination is the principal factor related to death by this disease. Breast cancer stem cells, are thought to be responsible for metastasis and chemoresistance.. In this study, based on whole transcriptome analysis from putative breast CSCs and reverse-engineering of transcription control networks, we were able to identify two networks associated to this phenotype.
2016-12-31 | GSE83811 | GEO
Project description:RUNX transciption factor mediated control of breast cancer stem cells
| PRJNA593717 | ENA
Project description:The eukaryotic elongation factor-2 kinase, eEF2K, restricts protein translation elongation, and was identified as a potential therapeutic target for diverse types of cancers including triple negative breast cancer (TNBC; PMID: 25330770). We have recently found that inhibition of eEF2K synergizes with depletion of eukaryotic translation initiation factor 4E-binding protein 1 (eIF4EBP1; 4E-BP1), a suppressor of eukaryotic protein translation initiation factor 4E (eIF4E), leading to effective growth suppression of TNBC cells in culture. We performed LC-MS/MS analysis following depletion of eEF2K and/or 4EBP in a TNBC cell line, Hs578t (YoungJun Ju & Eldad Zacksenhaus, manuscript in revisions). Depletion of these factors had overlapping effects on the proteome with the highest impact on Collagen containing extracellular matrix (e.g. COL1A1). The complete LC-MS/MS data sets (control vehicle; eEF2K-depletion, 4EBP1-depletion; combined eEF2k plus 4EBP1-depletion) are provided herein.
| MSV000086059 | MassIVE
Project description:Dysregulation of pathways due to mutations on oncogenes or tumor suppressors that leads to aberrant expression or activity of proteins is the most well understood mechanism that drives cancer initiation and progression. TRIB3, a member of the Tribbles family of pseudokinases, is often found dysregulated in cancer and has been associated with breast cancer initiation and metastasis formation. However, the underlying mechanisms by which TRIB3 contributes to these events are far from being understood. In contrast PPAR, a well-known transcription factor that belongs to the superfamily of nuclear receptors, has gained attention in recent years as drug target in breast cancer. PPAR possess anti-proliferative abilities and inducing its expression has been shown beneficial in different cancer models. In this study, we demonstrated that TRIB3 regulates PPAR expression in breast cancer cells and that TRIB3 interacts with the WRAD complex in these cells. We showed that TRIB3 expression influence H3K4me3 levels genome wide and specifically at the PPARG locus. All in all, our study situates TRIB3 as a new epigenetic regulator and represents a new line of research for the Tribbles scientific community, opening the door for future targeted therapeutic interventions for breast cancer patients
2022-10-13 | PXD036341 | Pride
Project description:Maintenance and propagation of breast cancer stem cells (BCSCs) is mediated via cytokine and growth factor networks. Direct in vivo linkage between dietary regulation of mammary stem (MaSC)/progenitor cell numbers and protection from breast cancer has not been reported. Here, we investigated the effect of post-weaning intake of soy protein isolate (SPI) relative to the control casein (CAS) diet on the stem/progenitor population and tumor formation in MMTV-Wnt1-Transgenic (Wnt1-Tg) female mice. Gene expression profile of the basal (MaSC-enriched) sub-population in preneoplastic Wnt1-Tg mice demonstrated a stem cell-like expression pattern and markedly suppressed expression of inflammatory cytokines, C-X-C family chemokines, and metastasis-associated genes with dietary SPI exposure. four Samples: two CAS diet, two SPI diet
2014-06-30 | E-GEOD-37849 | biostudies-arrayexpress
Project description:Embryonic stem cells have a unique regulatory circuitry, largely controlled by the transcription factors Oct4, Sox2 and Nanog, which generates a gene expression program necessary for pluripotency and self-renewal (Boyer et al. 2005; Loh et al. 2006; Chambers et al. 2003; Mitsui et al. 2003; Nichols et al. 1998). How external signals connect to this regulatory circuitry to influence embryonic stem cell fate is not known. We report here that a terminal component of the canonical Wnt pathway in embryonic stem cells, the transcription factor Tcf3, co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog. Thus Tcf3 is an integral component of the core regulatory circuitry of ES cells, which includes an autoregulatory loop involving the pluripotency regulators. Both Tcf3 depletion and Wnt pathway activation cause increased expression of Oct4, Nanog and other pluripotency factors and enhance pluripotency and self-renewal. Our results reveal that the Wnt pathway, through Tcf3, brings developmental signals directly to the core regulatory circuitry of ES cells to influence the balance between pluripotency and differentiation.
2008-02-28 | E-TABM-409 | biostudies-arrayexpress
Project description:The TCF3-HLF translocation is a very rare rearrangement in ALL that is associated with an extremely poor prognosis. The TCF3-HLF fusion gene in the described case resulted in the fusion of the homeobox-related gene of TCF3 to the leucine zipper domain of HLF. The TCF3-HLF fusion gene product acts as a transcriptional factor leading to the dedifferentiation of mature B lymphocytes into an immature state (lymphoid stem cells). This process initiates the formation of pre-leukaemic cells. Due to the rarity of this chromosomal aberration, only a few cases have been described in the literature. The advantage of this work is the presentation of an interesting case of clonal evolution of cancer cells and the cumulative implications (diagnostic and prognostic) of the patient’s genetic alterations.
2020-03-20 | GSE147280 | GEO