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...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2006-09, Vol.348 (2), p.600-605
Main Authors: Hong, Jie, Zhao, Yingchun, Huang, Weida
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
Antineoplastic Combined Chemotherapy Protocols - therapeutic use
B16 melanoma
Cell Line, Tumor
CELL PROLIFERATION
Cell Proliferation - drug effects
Combined treatment
ENZYMES
Escherichia coli
Escherichia coli - genetics
Escherichia coli - metabolism
esiRNA
INHIBITION
Melanoma, Experimental - drug therapy
MELANOMAS
MICE
ONCOGENES
Proto-Oncogene Proteins c-myc - antagonists & inhibitors
Proto-Oncogene Proteins c-myc - biosynthesis
RNA
RNA interference
RNA, Small Interfering - pharmacology
STAT3 Transcription Factor - antagonists & inhibitors
STAT3 Transcription Factor - biosynthesis
THERAPY
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.07.107