Similar Datasets
Project description:Bulk RNA Sequencing Analysis on the Effects of SIX2 Knock Down on Stem Cell Derived Beta cells.
| PRJNA616289 | ENA
Project description:Transcriptomic profiling by high-throughput sequencing of primary human Beta cells following SIX2 or SIX3 loss of function. SIX2 genome-binding profiling by CUT&RUN and high-throughput sequencing. This SuperSeries is composed of the SubSeries listed below.
2021-01-26 | GSE164628 | GEO
Project description:Transcriptomic profiling by high-throughput sequencing of primary human Beta cells following SIX2 or SIX3 loss of function.
2021-01-26 | GSE164626 | GEO
Project description:Purpose: Bulk transcriptomics analysis of Wilms tumor SIX2+CITED1+ cells to compare and identify unique nephron progenitor transcriptome profiling (RNA-seq) signature between unfavorable and favorable Wilms Tumors and against human fetal kidney Methods: Wilms tumor samples were collected and transported on ice at 4°C in RPMI-1640 and a single cell suspensions were prepared following mechanical and enzymatic dissociation as previously publication. Enzymatic dissociation was performed with 125 U/ml collagenase I in RPMI-1640 at 37 °C for 35 min. The digested cells were then passed through a 100-μm cell strainer and a 40-μm cell strainer with washes of 1x PBS. The cell suspension was than centrifuged at 1500 rpm for 5 min and erythrocytes were eliminated using a red blood cell lysis kit. WT SIX2+CITED1+ cells were isolated using SIX2-Cy5 and CITED1-Cy3 Smartflare RNA probes following manufacturer’s instructions and previous publication. Briefly, cells were incubated over night at 37 °C with both RNA probes diluted at 1:20 in PBS and 25ul/ml in RPMI-1640 supplemented with 5% FBS, and 0.2% antimicrobial agent Primocin. After 16-18 h, cells were dissociation using TrypLE 1x for 5 min, cells were centrifuged at 1500 rpm for 5 min and prepared for FACS. RNA extraction was performed immediately after FACS using the RNeasy Micro Kit following manufacturer’s recommendations. After cDNA production and construction of DNA libraries, the samples were run on an Illumina NextSep500 (Illumina). Differential gene expression was analyzed using ERCC ExFold probes with the Remove Unwanted Variation R/Bioconductor software package combined with edgeR Results: Transcriptomics analysis of Wilms Tumor SIX2+CITED1+ cells in comparison to different tumor types and human fetal kidneys confirmed the nephrogenic signature of hFK-SIX2+CITED1+ and WT-SIX2+CITED1+ cells but highlighted differences in expression of pluripotency and self renewal-related genes like OCT4, FOXO1, SALL, NANOG along with a lower expression of β-catenin, TCF, and other growth factors known to promote differentiation (BMPs, FGFs). Hierarchical clustering of gene expression showed shared similarities between Wilms tumor samples against human fetal kidney samples however, with major differences in gene expression between tumor-to-tumor type was also present. Conclusion: Our study represents the first transcriptomic characterization of Wilms Tumor cancer stem cells (SIX2+CITED1+) against human fetal kidney SIX2+CITED1+ cells. Identifying specify gene expression and signaling pathway profiles across different subtypes of Wilms Tumor and against human fetal kidney SIX2+CITED1+ cells.
2024-01-08 | GSE176342 | GEO
Project description:The use of androgen receptor (AR) inhibitors in prostate cancer gives rise to increased cellular lineage plasticity resulting resistance to AR-targeted therapies. By examining the chromatin landscape of AR positive prostate cancer cells following exposure to the AR inhibitor enzalutamide, we have identified a novel regulator of cell plasticity, homeobox transcription factor SIX2, whose motif is enriched in accessible regions post-treatment. Our investigation demonstrates that depletion of SIX2 in androgen-independent PC-3 prostate cancer cells is sufficient to induce a switch from a stem-like to an epithelial state, leading to the reduction of key cancer-related properties such as proliferation, colony formation, and metastasis both in vitro and in vivo. These effects are mediated through downregulation of Wnt/β-catenin signalling pathway and subsequent reduced nuclear localization of β-catenin. Collectively, our findings provide compelling evidence that depletion of SIX2 may represent a promising strategy for overcoming cell plasticity mechanisms driving AR resistance in prostate cancer.
2024-03-19 | GSE235956 | GEO
Project description:The use of androgen receptor (AR) inhibitors in prostate cancer gives rise to increased cellular lineage plasticity resulting resistance to AR-targeted therapies. By examining the chromatin landscape of AR positive prostate cancer cells following exposure to the AR inhibitor enzalutamide, we have identified a novel regulator of cell plasticity, homeobox transcription factor SIX2, whose motif is enriched in accessible regions post-treatment. Our investigation demonstrates that depletion of SIX2 in androgen-independent PC-3 prostate cancer cells is sufficient to induce a switch from a stem-like to an epithelial state, leading to the reduction of key cancer-related properties such as proliferation, colony formation, and metastasis both in vitro and in vivo. These effects are mediated through downregulation of Wnt/β-catenin signalling pathway and subsequent reduced nuclear localization of β-catenin. Collectively, our findings provide compelling evidence that depletion of SIX2 may represent a promising strategy for overcoming cell plasticity mechanisms driving AR resistance in prostate cancer.
2024-03-19 | GSE235955 | GEO
Project description:The use of androgen receptor (AR) inhibitors in prostate cancer gives rise to increased cellular lineage plasticity resulting resistance to AR-targeted therapies. By examining the chromatin landscape of AR positive prostate cancer cells following exposure to the AR inhibitor enzalutamide, we have identified a novel regulator of cell plasticity, homeobox transcription factor SIX2, whose motif is enriched in accessible regions post-treatment. Our investigation demonstrates that depletion of SIX2 in androgen-independent PC-3 prostate cancer cells is sufficient to induce a switch from a stem-like to an epithelial state, leading to the reduction of key cancer-related properties such as proliferation, colony formation, and metastasis both in vitro and in vivo. These effects are mediated through downregulation of Wnt/β-catenin signalling pathway and subsequent reduced nuclear localization of β-catenin. Collectively, our findings provide compelling evidence that depletion of SIX2 may represent a promising strategy for overcoming cell plasticity mechanisms driving AR resistance in prostate cancer.
2024-03-19 | GSE235957 | GEO
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
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
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