Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1135734 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29825300_1.fastq.gz | Fastqsanger.gz | |||
| SRR29825300_2.fastq.gz | Fastqsanger.gz | |||
| SRR29825301_1.fastq.gz | Fastqsanger.gz | |||
| SRR29825301_2.fastq.gz | Fastqsanger.gz | |||
| SRR29825302_1.fastq.gz | Fastqsanger.gz |
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Project description:Our main research focuses on the intervention of iodine-125 radioactive particles on liver cancer cells, inducing changes in gene expression, which may affect changes in biological characteristics. This provides clues for the potential mechanisms of iodine-125 radioactive particle therapy in liver cancer and offers new targets for disease treatment.
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Project description:After being irradiated with iodine-125 particles, the proteomic alterations in HCC xenografts .
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Project description:Whole genome microarray data were analyzed to describe the changes in gene transcription profile in human Caco-2 cancer cells under the influence of the extract from iodine-biofortified and non-fortified carrot and lettuce. These iodine-biofortified vegetables can be used as a functional food. Four-condition experiment: iodine-biofortified carrot, non-fortified carrot, iodine-biofortified lettuce, non-fortified lettuce vs. Caco-2 colorectal adenocarcinoma cell line. Three biological replicates and three technical replicates.
2015-08-01 | E-GEOD-71605 | biostudies-arrayexpress
Project description:Whole genome microarray data were analyzed to describe the changes in gene transcription profile in human Caco-2 cancer cells under the influence of the extract from iodine-biofortified and non-fortified carrot and lettuce. These iodine-biofortified vegetables can be used as a functional food.
2015-08-01 | GSE71605 | GEO
Project description:RNA-binding proteins (RBPs) are critical regulators of gene expression, but only a small fraction have been studied for their role in malignancy. Here we report a systematic analysis of RBP CUGBP Elav-Like Family member 1 (CELF1 alias CUGBP1) roles in mRNA alternative splicing, translation and turnover in oral cancer cells. CELF1 is overexpressed in carcinogen-induced oral cancer tumorigenesis mouse model and specific inhibition of CELF1 reduces tumor growth in vivo. Deep transcriptomic analysis revealed that hundreds of mRNAs were differentially regulated as a function of CELF1 expression in oral cancer cells. More importantly, the presence of CELF1 promoted alternative splicing of several target mRNAs which are known to be involved in various cancer biological processes. Using a pulse SILAC-based quantitative proteomic approach, we observed hundreds of proteins whose translation was controlled by CELF1 and those altered proteins were implicated in malignancy. Altogether, these data provided a comprehensive view of the CELF1 mRNA regulatory network in OSCC and suggests that CELF1 is a viable target for therapeutic intervention. Significance Post-transcriptional mechanisms that regulate cancer cells which are believed to constitute the driving force of many malignancies are poorly understood. We show that oral squamous cell carcinoma (OSCC) emerge as a result of an over expressed RNA-binding protein CELF1, a protein implicated in mRNA turnover, alternative splicing and translation. The resulting mRNA expression repertoire regulates networks of genes whose expression changes regulate oral cancer pathogenesis. Inhibition of CELF1 mitigated OSCC tumor-forming capacity and offers an attractive therapeutic option for oral malignancies. Transcriptomic analysis of UMSCC-74B oral cancer cells as a function of CELF1 protein expression.
2015-09-01 | E-GEOD-57254 | biostudies-arrayexpress
Project description:OBJECTIVE: Nonalcoholic steatohepatitis (NASH) is closely associated with metabolic syndrome and increases the risk for end-stage liver disease, such as cirrhosis and hepatocellular carcinoma. Despite this, the molecular events that influence NASH pathogenesis remain poorly understood. The objectives of the current study are to delineate the transcriptomic and proteomic signatures of NASH liver, to identify potential pathogenic pathways and factors, and to critically assess their role in NASH pathogenesis. METHODS: We performed RNA sequencing and quantitative proteomic analyses on the livers from healthy and diet-induced NASH mice. We examined the association between plasma levels of TSK, a newly discovered hepatokine, and NASH pathologies and reversal in response to dietary switch in mice. Using TSK knockout mouse model, we determined how TSK deficiency modulates key aspects of NASH pathogenesis. RESULTS: RNA sequencing and quantitative proteomic analyses revealed that diet-induced NASH triggers concordant reprogramming of the liver transcriptome and proteome in mice. NASH pathogenesis is linked to elevated plasma levels of the hepatokine TSK, whereas dietary switch reverses NASH pathologies and reduces circulating TSK concentrations. Finally, TSK inactivation protects mice from diet-induced NASH and liver transcriptome remodeling. CONCLUSIONS: Global transcriptomic and proteomic profiling of healthy and NASH livers revealed the molecular signatures of diet-induced NASH and dysregulation of the liver secretome. Our study illustrates a novel pathogenic mechanism through which elevated TSK in circulation promotes NASH pathologies, thereby revealing a potential target for therapeutic intervention.
2019-01-08 | GSE119340 | GEO
Project description:The GEMINAL Study- Gene Expression Modulation by Intervention with Nutrition and Lifestyle We conducted a pilot study to examine changes in gene expression in men diagnosed with low risk prostate cancer who participated in an intensive nutrition and lifestyle intervention. We profiled gene expression in morphologically normal tissues from prostate biopsies of all 30 participants before and after the intervention. Keywords: Differential gene expression analysis Pre-intervention versus Post-Intervention
2010-05-26 | E-GEOD-10306 | biostudies-arrayexpress
Project description:Perchlorate, which is a ubiquitous and persistent ion, competitively interferes with iodide accumulation in the thyroid, causing iodine deficiency, which may result in reduced thyroid hormone synthesis and secretion. Human studies suggest that perchlorate presents very little risk in healthy individuals; however, the precautionary principle demands that the sensitive populations of iodine deficient adults and mothers require extra consideration. In an attempt to determine if the effects on gene expression were similar, we compared the thyroidal effects of perchlorate (10 mg/kg) treatment for 14 days in drinking water with those caused by 8 weeks of Iodine-deficiency in rats. The thyroids were collected (N=3 each group) and total mRNA was analyzed using the Affymetrix Rat Genome 230 2.0 GeneChip®. Changes in gene expression were compared with appropriate control groups. We compared the 2-fold gene changes due to I-deficiency with changes due to perchlorate treatment. 189 transcripts were changed by the Iodine-deficient diet and 722 transcripts were changed by the perchlorate treatment. 34% of the transcripts changed by the I-deficient diet were also changed by perchlorate and generally in the same direction. three specific transporter genes, AQP1, NIS, & SLC22A3 were changed by both treatments, indicating that the membrane specific changes were similar. Iodine-deficiency primarily caused changes in retinol and calcium signaling pathways and perchlorate primarily caused changes related to the accumulation of extracellular matrix proteins. This study provides evidence that perchlorate, at least at this dose level, changes more genes and changes different genes compared to iodine deficiency.
2010-11-04 | GSE25144 | GEO
Project description:Transcriptomic analysis of breast cancer tumors treated with iodine
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Project description:Combining the results of a large scale proteomic analysis of human transcription factor interaction network with knowledge databases, we identified FOXR2 as one of the top-ranked candidate proto-oncogenes. Here, we show that FOXR2 forms a stable complex with MYC and MAX and subsequently regulates cell proliferation by promoting MYC’s transcriptional activities. We demonstrated that FOXR2 is highly expressed in several breast, lung, and liver cancer cell lines and related patient tumor samples, while reduction of FOXR2 expression in a xenograft model inhibits tumor growth. These results indicate that FOXR2 acts with MYC to promote cancer cell proliferation, which is a potential tumor-specific target for therapeutic intervention against MYC-driven cancers.
2017-02-17 | GSE81381 | GEO