RNAi Based Approaches to the Treatment of Malignant Glioma
Open Access
- 1 June 2006
- journal article
- research article
- Published by SAGE Publications in Technology in Cancer Research & Treatment
- Vol. 5 (3) , 261-269
- https://doi.org/10.1177/153303460600500313
Abstract
RNA interference (RNAi) is a recently discovered, powerful molecular mechanism that can be harnessed to engineer gene-specific silencing in mammalian tissues. A mechanism, where short double-stranded RNA (dsRNA) molecules, when introduced into cells elicit specific “knock-down” of gene expression via degradation of targeted messenger RNA, has lately become the technique of choice for analysis of gene function in oncology research. Thus, RNAi is currently being extensively evaluated as a potential therapeutic strategy against malignant gliomas, since surgical, radiological, and chemotherapeutic interventions during the past few decades have done little to improve the poor prognosis rate for patients with these dreaded tumors. This review summarizes the pre-clinical studies that are currently underway to test the validity of RNAi as a potential therapeutic strategy against malignant gliomas, and discusses the potential technical Hurdles that remain to be overcome before the technique can become a promising clinical therapy to combat this frequently lethal disease.Keywords
This publication has 80 references indexed in Scilit:
- Downregulation of Apaf-1 and caspase-3 by RNA interference in human glioma cells: Consequences for erucylphosphocholine-induced apoptosisApoptosis, 2005
- RNAi: The Nuts and Bolts of the RISC MachineCell, 2005
- Phorbol 12-Myristate 13-Acetate Induces Epidermal Growth Factor Receptor Transactivation via Protein Kinase Cδ/c-Src Pathways in Glioblastoma CellsJournal of Biological Chemistry, 2005
- Deficiency in the Catalytic Subunit of DNA-Dependent Protein Kinase Causes Down-Regulation of ATMCancer Research, 2005
- RNA interference against a glioma-derived allele of EGFR induces blockade at G2MOncogene, 2004
- Overexpression of RFT induces G1–S arrest and apoptosis via p53/p21Waf1 pathway in glioma cellBiochemical and Biophysical Research Communications, 2004
- Physical and functional interaction between BH3-only protein Hrk and mitochondrial pore-forming protein p32Cell Death & Differentiation, 2004
- In vivo knockdown of gene expression in brain cancer with intravenous RNAi in adult ratsThe Journal of Gene Medicine, 2003
- Induction of an interferon response by RNAi vectors in mammalian cellsNature Genetics, 2003
- U6 promoter–driven siRNAs with four uridine 3′ overhangs efficiently suppress targeted gene expression in mammalian cellsNature Biotechnology, 2002