Blocking c-myc and stat3 by E. coli expressed and enzyme digested siRNA in mouse melanoma.
Tumour cells often show alteration in the signal-transduction pathways, leading to proliferation in response to external signals. Oncogene overexpression and constitutive expression is a common phenomenon in the development and progression of many human cancers. Therefore oncogenes provide potential targets for cancer therapy. RNA interference (RNAi), mediated by small interfering RNA (siRNA), silences genes with a high degree of specificity and potentially represents a general approach for molecularly targeted anti-cancer therapy. The data presented in this report evaluated the method of systemically administering combined esiRNAs to multiple targets as compared with the method of using a single kind of esiRNA to a single target. Our experimental data revealed that the mixed treatment of esiC-MYC and esiSTAT3 had a better inhibition effect than the single treatment of esiC-MYC or esiSTAT3 on mouse B16 melanoma.
Hong
Jie
J
Department of Biochemistry, School of Life Sciences, Fudan University, Shanghai 200433, China.
Zhao
Yingchun
Y
Huang
Weida
W
D000818:Animals; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004926:Escherichia coli / Q000235:genetics / Q000378:metabolism; D008546:Melanoma, Experimental / Q000188:drug therapy; D051379:Mice; D016271:Proto-Oncogene Proteins c-myc / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D034741:RNA, Small Interfering / Q000494:pharmacology*; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors* / Q000096:biosynthesis
D016271:Proto-Oncogene Proteins c-myc; D034741:RNA, Small Interfering; D050796:STAT3 Transcription Factor