These results may be accounted for by different posttranscriptional regulatory mechanisms. Main tumors and their several developmental phases can now be characterized molecularly by comparative whole genome expression profiling, the use of chips for mRNA detection, and proteomic methods. MicroRNA expression in tumors was not long ago shown to supply valid unique signatures for every kind of tumor. The research of other kinds of regulatory RNAs might possibly maximize the accuracy of molecular characterization for every tumor. Distinctive posttranscriptional regulation of ETS one and ETS two mRNAs by distinct microRNAs and/or RNA binding proteins could possibly explain our findings. Our observations could also be explained by epigenetic alterations in tumor cells possessing differential results over the regulation of genes encoding transcription components and/or cotranscriptional regulators of ETS one and ETS 2.
Even more experiments are needed to check these hypotheses. Such as, the position of Protein Kinase C should selleck be explored given that it is actually implicated in cell proliferation, cell migration, and tumor cell invasion in melanoma and increases the stability within the ETS 1 protein. One particular purpose for ETS one and ETS 2 in ocular cancer and choroidal melanoma could possibly be mediated via their improved transcriptional exercise and upregulated expression of recommended you read their target genes associated with angiogenesis and/or metastatic propagation. ETS one and ETS two are activated by phosphorylation by way of Ras/mitogen activated protein kinase signaling but may also be repressed by serine phosphorylation. Lively ETS proteins can transactivate targeted genes. We studied the expression of target genes encoding ICAM one, PAI one, MCP 1, and p16 to find out the prospective roles of ETS one and ETS 2 inside the improvement of this tumor.
We demonstrated by semi quantitative RT PCR that ETS one and ETS two target genes have been upregulated from P20 towards the age of three months in these mice, constant with our

observations for ETS one and ETS 2 mRNA and protein ranges. These findings strongly propose that both ETS one and ETS two are upregulated in this mouse model of ocular tumor with increased levels of transcriptional activity than in control mice. These effects could possibly be involved with the pathogenic mechanisms of this sickness. Most ETS aspects are oncogenic, plus the upregulation of ETS gene expression is described in many types of human tumors. The levels of expression of those genes are correlated with invasion and metastasis and may possibly be handy for predicting tumor progression in cancer individuals.