These effects may be accounted for by various posttranscriptional regulatory mechanisms. Primary tumors and their several developmental phases can now be characterized molecularly by comparative complete genome expression profiling, the usage of chips for mRNA detection, and proteomic approaches. MicroRNA expression in tumors was not too long ago shown to supply legitimate distinct signatures for each form of tumor. The examine of other varieties of regulatory RNAs may possibly grow the accuracy of molecular characterization for each tumor. Different posttranscriptional regulation of ETS 1 and ETS two mRNAs by distinct microRNAs and/or RNA binding proteins could probably describe our findings. Our observations could also be explained by epigenetic adjustments in tumor cells acquiring differential results to the regulation of genes encoding transcription variables and/or cotranscriptional regulators of ETS 1 and ETS 2.
Even further experiments are required to test these hypotheses. Such as, the function of Protein Kinase C should really describes it be explored simply because it can be implicated in cell proliferation, cell migration, and tumor cell invasion in melanoma and increases the stability within the ETS one protein. A single part for ETS one and ETS two in ocular cancer and choroidal melanoma might be mediated as a result of their increased transcriptional activity and upregulated expression of smad inhibitor their target genes involved in angiogenesis and/or metastatic propagation. ETS 1 and ETS two are activated by phosphorylation by Ras/mitogen activated protein kinase signaling but may also be repressed by serine phosphorylation. Active ETS proteins can transactivate targeted genes. We studied the expression of target genes encoding ICAM 1, PAI one, MCP 1, and p16 to find out the possible roles of ETS one and ETS 2 inside the advancement of this tumor.
We demonstrated by semi quantitative RT PCR that ETS 1 and ETS two target genes have been upregulated from P20 to your age of 3 months in these mice, steady with our

observations for ETS one and ETS two mRNA and protein levels. These findings strongly propose that each ETS one and ETS two are upregulated on this mouse model of ocular tumor with larger levels of transcriptional exercise than in manage mice. These effects could possibly be involved with the pathogenic mechanisms of this disease. Most ETS things are oncogenic, plus the upregulation of ETS gene expression has been described in many sorts of human tumors. The amounts of expression of those genes are correlated with invasion and metastasis and could be practical for predicting tumor progression in cancer individuals.