SOX2 Mediates Metabolic Reprogramming of Prostate Cancer Cells (ChIP-Seq)
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PROVIDER: PRJNA699550 | ENA |
REPOSITORIES: ENA
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Project description:SOX2 Mediates Metabolic Reprogramming of Prostate Cancer Cells
| PRJNA699549 | ENA
Project description:SOX2 Mediates Metabolic Reprogramming of Prostate Cancer Cells (RNA-Seq)
| PRJNA699551 | ENA
Project description:To mechanistically define the function of SOX2 in prostate cancer cells and how it contributes to therapeutic resistance, we performed paired SOX2 chromatin immunoprecipitation-sequencing (ChIP-Seq) and RNA-sequencing (RNA-Seq) on a SOX2-positive CRPC cell line, CWR-R1, to determine which genes SOX2 binds and potentially regulates. To identify novel prostate cancer-specific SOX2 gene targets in CRPC cells distinct from known SOX2 stem cell genes, we conducted parallel SOX2 ChIP-Seq and RNA-Seq in the WA01 embryonic stem cell line and compared results to identified SOX2 targets from CWR-R1 cells
2022-01-26 | GSE166183 | GEO
Project description:To determine the genes regulated by SOX2, we performed RNA-Seq on CWR-R1 control cells and SOX2KO cells with intact AR signaling and identified differentially expressed genes (DEGs)
2022-01-26 | GSE166184 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-01-24 | GSE166185 | GEO
Project description:Androgens are central to prostate cancer (PCa) development and targeting this pathway is currently the main therapeutic axis in the clinic, but the mechanism by which androgen signaling contributes to the oncometabolic state of PCa cells remains to be fully elucidated. The intersection of gene expression, binding-events and motif finding analyses following androgen exposure identified a metabolic gene signature associated with the action of estrogen-related receptors (ERRs). Unexpectedly, we show that ERRγ acts as a negative regulator of mitochondrial respiration in the context of PCa, and that AR-dependent direct repression of ERRγ promotes the reactivation of a functional TCA cycle. This metabolic state, which parallels the loss of ERRγ expression, was observed in both androgen-dependent and castration-resistant PCa and was associated with cell proliferation. Interrogation of several clinical studies revealed a strong inverse relationship between ERRγ expression and the severity of the disease. Our study uncovers a novel mechanism by which AR-dependent repression of ERRγ contributes to the reprogramming of PCa cell metabolism to favor mitochondrial activity and cell proliferation. We used microarrays to investigate the transcriptional regulation of metabolic genes by 72h treatment with R1881, a synthetic androgens, with or without repression of the estrogen-related receptor gamma, in LNCaP prostate cancer cells.
2016-12-06 | GSE86781 | GEO
Project description:Pluripotent stem cell lines derived from embryos of different stages have distinct pluripotent ground states, but similar levels of the transcription factor Oct4. Epiblast-derived pluripotent stem cells (EpiSCs), in contrast to embryonic stem (ES) cells, cannot form chimeras. We show that EpiSCs express lower levels of the transcription factors Sox2 and Klf4 than ES cells and have limited reprogramming potential, as shown by cell fusion. Sox2 overexpression dramatically increases the reprogramming potential, chimera formation, and germline contribution of EpiSCs. Therefore, although Oct4 is essential for reprogramming, the level of Sox2 defines both the reprogramming capability and the pluripotent ground states. RNA samples to be analyzed on microarrays were prepared using Qiagen RNeasy columns with on-column DNA digestion. 300 ng of total RNA per sample was used as input into a linear amplification protocol (Ambion), which involved synthesis of T7-linked double-stranded cDNA and 12 hrs of in-vitro transcription incorporating biotin-labelled nucleotides. Purified and labelled cRNA was then hybridized for 18 hrs onto MouseRef-8 v2 expression BeadChips (Illumina) according to the manufacturer's instructions. After washing, as recommended, chips were stained with streptavidin-Cy3 (GE Healthcare) and scanned using the iScan reader (Illumina) and accompanying software. Samples were hybridized as biological replicates. 12 sample types were analyzed, each of them in duplicate. ESCm: Mouse ESC male; ESCf: Mouse ESC OG2 female; F9 EC: F9 EC (mouse embryonic carcinoma cell); F9-Sox2: F9 EC (mouse embryonic carcinoma cell) overexpressing wild type Sox2; EpiSCf: Mouse EpiSC OG2 female; Epi-Sox2f: Mouse EpiSC Sox2 (OG2 female) overexpressing wild type Sox2; P19 EC: P19 EC (mouse embryonic carcinoma cell); P19-Sox2: P19 EC (mouse embryonic carcinoma cell) overexpressing wild type Sox2; EpiSCm: Mouse EpiSC (GOF18 male) (duplicates); EpiSox2mL2: Mouse EpiSC Sox2 (GOF18 male) overexpressing wild type Sox2 cultured in condition EpiSC medium (CM); EpiSox2mE1: Mouse EpiSC Sox2 (GOF18 male) overexpressing wild type Sox2 cultured in ESC medium (ESC like1); EpiSox2mE2: Mouse EpiSC Sox2 (GOF18 male) overexpressing wild type Sox2 cultured in ESC medium (ESC like2).
2010-12-31 | E-GEOD-15358 | biostudies-arrayexpress
Project description:Metabolic reprogramming and energetic rewiring are hallmarks of cancer which fuel disease progression and facilitate evasion to the rising anti-tumour pressures introduced by therapy. The remodelling of oxidative phosphorylation and enhanced lipogenesis have previously been characterised as key metabolic features of prostate cancer (PCa). Recently, succinate-dependent mitochondrial reprogramming was identified in high-grade PCa tumours, as well as upregulation of the enzymes associated with branched-chain amino acid (BCAA) catabolism. In this study, we hypothesised that the degradation of the BCAAs, particularly valine, may play a critical role in anapleurotic refuelling of the mitochondrial succinate pool, as well as the maintenance of intracellular lipids in PCa.
2024-01-18 | GSE253413 | GEO
Project description:SOX2 and OCT4, in conjunction with KLF4 and cMYC, are sufficient to reprogram human fibroblasts to induced pluripotent stem cells (iPSCs), but it is unclear if they function as transcriptional activators or as repressors. We now show that, like OCT4, SOX2 functions as a transcriptional activator. We substituted SOX2-VP16 (a strong activator) for wild-type (WT) SOX2, and we saw an increase in the efficiency and rate of reprogramming, whereas the SOX2-HP1 fusion (a strong repressor) eliminated reprogramming. We report that, at an early stage of reprogramming, virtually all DNA-bound OCT4, SOX2, and SOX2-VP16 were embedded in putative enhancers, about half of which were created de novo. Those associated with SOX2-VP16 were, on average, stronger than those bearing WT SOX2. Many newly created putative enhancers were transient, and many transcription factor locations on DNA changed as reprogramming progressed. These results are consistent with the idea that, during reprogramming, there is an intermediate state that is distinct from both parental cells and iPSCs.
2017-08-30 | GSE81900 | GEO
Project description:SOX2 and OCT4, in conjunction with KLF4 and cMYC, are sufficient to reprogram human fibroblasts to induced pluripotent stem cells (iPSCs), but it is unclear if they function as transcriptional activators or as repressors. We now show that, like OCT4, SOX2 functions as a transcriptional activator. We substituted SOX2-VP16 (a strong activator) for wild-type (WT) SOX2, and we saw an increase in the efficiency and rate of reprogramming, whereas the SOX2-HP1 fusion (a strong repressor) eliminated reprogramming. We report that, at an early stage of reprogramming, virtually all DNA-bound OCT4, SOX2, and SOX2-VP16 were embedded in putative enhancers, about half of which were created de novo. Those associated with SOX2-VP16 were, on average, stronger than those bearing WT SOX2. Many newly created putative enhancers were transient, and many transcription factor locations on DNA changed as reprogramming progressed. These results are consistent with the idea that, during reprogramming, there is an intermediate state that is distinct from both parental cells and iPSCs
2017-08-30 | GSE81899 | GEO