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pmid: 17658462
Knockdown of c-myc expression via RNAi is expected to be an efficient approach to suppress tumor growth. In our preliminary study, we intraperitoneally injected different doses of c-myc-directed esiRNA (esic-MYC, c-myc-directed Escherichia coli expressed and enzyme digested siRNA) into C57BL6/6J mice with bearing B16 melanoma to investigate the inhibitory effect of esic-MYC on tumor growth. However, in high dose esic-MYC treatment groups, the tumor growth inhibition was less efficient than that of low dose treatment groups. Considering the negative regulation roles of eri-1 and adar-1 genes in RNA interference, we downregulated either/both of the two genes with c-myc gene by RNAi. Our results showed esiMERI-1 (esiRNA of mouse eri-1 gene) and esiMADAR-1 (esiRNA of mouse adar-1 gene) could rescue the tumor growth suppression in the high dose esic-MYC treatment groups obviously. The data strongly suggest that silencing of eri-1 and adar-1 homologs of human being should be concerned for cancer therapy by RNAi approach.
Exonucleases, Adenosine Deaminase, Melanoma, Experimental, RNA-Binding Proteins, Apoptosis, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Mice, Exoribonucleases, In Situ Nick-End Labeling, Animals, RNA Interference, RNA, Messenger, RNA, Small Interfering, Cell Proliferation
Exonucleases, Adenosine Deaminase, Melanoma, Experimental, RNA-Binding Proteins, Apoptosis, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Mice, Exoribonucleases, In Situ Nick-End Labeling, Animals, RNA Interference, RNA, Messenger, RNA, Small Interfering, Cell Proliferation
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