Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

CHSA transcriptional profiles

ABSTRACT: Transcriptional profiling of preangiogenic and angiogenic tumor nodules was conducted to identify genes that were differentially expressed during the transition from the preangiogenic to the angiogenic phenotype.

ORGANISM(S): Rattus norvegicus

DISEASE(S): angiogenic chondrosarcoma

SUBMITTER: Di Jia

PROVIDER: E-MEXP-3775 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Transcriptional repression of VEGF by ZNF24: mechanistic studies and vascular consequences in vivo.

Jia Di D Hasso Sean M SM Chan Joanne J Filingeri Domenic D D'Amore Patricia A PA Rice Lori L Pampo Christine C Siemann Dietmar W DW Zurakowski David D Rodig Scott J SJ Moses Marsha A MA

Blood 20121203 4

VEGF is a key regulator of normal and pathologic angiogenesis. Although many trans-activating factors of VEGF have been described, the transcriptional repression of VEGF remains much less understood. We have previously reported the identification of a SCAN domain-containing C2H2 zinc finger protein, ZNF24, that represses the transcription of VEGF. In the present study, we identify the mechanism by which ZNF24 represses VEGF transcription. Using reporter gene and electrophoretic mobility shift as ...[more]

PMID: 23212515

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Project description:A large body of evidence has demonstrated that many human tumors are maintained by a small cell population called cancer stem cells (CSCs) or tumor progenitors, which are responsible for tumor formation, therapy resistance and metastasis. We found that ionizing radiation treatment enriches for the CSC phenotype and properties by preferential survival and expansion of tumor progenitor cells. Our studies revealed that aldehyde dehydrogenase (ALDH) activity is indicative of prostate tumor progenitor cells with increased chemo- and radioresistance, enhanced migratory potential, improved DNA- double strand break repair and activation of the signaling pathways, which promote self-renewal and epithelial-mesenchymal transition. We found that X-ray irradiation can convert the bulk tumor cells to more clonogenic and radioresistant population positive for expression of CSC markers. For the first time we showed that irradiation increases histone H3K4 and H3K36 methylation in prostate cancer cells, thereby reactivating transcription of epigenetically silenced target genes. We showed that radioresistant tumor progenitor population undergoes a phenotypical switching during the course of irradiation, suggesting that controlling the phenotypical and functional properties of CSCs during radiation therapy is ultimative for the optimization of treatment strategies. Our studies have shown that CSC markers may be beneficial in prediction of tumor radiocurability, and combination of irradiation with therapies directed against CSCs can be a useful strategy to improve cancer treatment. To identify potential biomarkers associated with CSC population in these xenograft tumors, we performed whole genome gene expression profiling of the xenograft tumors treated with NVP-BEZ235, which eliminates prostate cancer progenitor populations or with Taxotere, which targets the bulk tumor cells as compared with vehicle-treated control mice. Treatment with either vehicle, Taxotere, NVP-BEZ235, or a combination of these two. There are no replicates

Dataset Information

CHSA transcriptional profiles

Publications

Transcriptional repression of VEGF by ZNF24: mechanistic studies and vascular consequences in vivo.

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