Unknown,Transcriptomics,Genomics,Proteomics

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Expression data for MCF-7 treated with PolII inhibitors, Triptolide or alpha-amanitin

ABSTRACT: Transcription of mRNA in mammalian is mainly performed by RNA polymerase II (PolII). POLRMT is responsible for the production of cytoplasmic and nuclear form of mitochondrial RNA polymerase. The former (mtRNAP) participates in transcription of RNA in the mitochondria while the latter (spRNAP-IV) is responsible for some mRNA transcription in the nucleus. The nature and amount of genes transcribed by spRNAP-IV still remains unclear. Thus, we scanned for possible candidate genes by using Affymetrix. MCF7 cells were cultured in RPMI medium supplemented with 10% fetal bovine serum. To determine the inhibition of PolII transcription, cells were cultured in the presence of 10 μg/ml of alpha-amanitin or 0.3μM of triptolide (Sigma) for 48 or 24 h, respectively.

ORGANISM(S): Homo sapiens

SUBMITTER: Ming-Ta Hsu

PROVIDER: E-GEOD-28444 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome. Methods:; Soleus gene expression of both sedentary and exercise trained HCR and LCR was characterized by microarray- and gene ontology analysis. Results: Although HCR and LCR had an inborn 347% difference in running capacity, only three genes were found differentially expressed in the soleus muscle between the two groups. Up-regulation of the mitochondrial enzyme leucyl-transferRNA synthetase (LARS2) was found in the sedentary LCR. Increased expression of LARS2 has been associated with a mitochondrial DNA mutation linked to maternally inherited diabetes and mitochondrial dysfunction. In line with our findings, a growing body of evidence suggests that LCR have compromised mitochondrial function. After exercise training, 58 genes were altered in the soleus muscle of HCR, in contrast to only one in the LCR group. This suggests that animals born with different levels of fitness respond different to the same type of exercise training. Adaptations to exercise in HCR seemed to be associated with increased lipid metabolism and fatty acid elongation in the mitochondria. Also, genes associated with the peroxisomes, seemed to be central in the adaptation to exercise. Conclusion: The results indicate that (i) LCR might have mitochondrial dysfunction, which may be a contributing factor of the low inborn aerobic capacity, (ii) animals born with different levels of fitness respond different to the same exercise program. Experiment Overall Design: There are 16 samples in this study.

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Expression data for MCF-7 treated with PolII inhibitors, Triptolide or alpha-amanitin

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