Suppression of EGFR expression by antisense RNA and RNAi

0Citations
Citations of this article
1Readers
Mendeley users who have this article in their library.
Get full text

Abstract

Glioblastoma is the most aggressive form of glioma, representing 15-20% of intracranial tumors and approximately half of gliomas in adults. Even though currently available combined therapy is used, the prognosis of patients with glioblastoma remains poor. In recent years, molecular targeted therapies have been developed when the molecular mechanism of glioblastomas is better understood. Epidermal growth factor receptor (EGFR) amplification/overexpression has been identified as the most common and important genetic aberration in glioblastomas, and it has become a prime target for molecular therapy of glioblastomas. In the present study, antisense EGFR RNA and EGFR siRNA were stably transfected into glioblastoma cells, resulting in significant suppression of EGFR expression, inhibition of cell viability and invasion, and induction of cell apoptosis both in vitro and in vivo. It seems that EGFR siRNA is more effective than antisense EGFR RNA. However, for obtaining high potency and favorable efficacy, the specific targeting site selection and screening are important when using either antisense EGFR RNA or EGFR siRNA treatment. It is expected that the delivery system with sufficiently high efficiency of transfection of antisense RNA and siRNA into tumor cells will be further developed. Combination of RNAi targeting multiple genes with conventional therapy will likely enhance the efficacy of glioblastoma treatment and will be a promising approach in the future.

Cite

CITATION STYLE

APA

Pu, P., Kang, C., & Jiang, H. (2009). Suppression of EGFR expression by antisense RNA and RNAi. In Therapeutic Ribonucleic Acids in Brain Tumors (pp. 407–424). Springer-Verlag Berlin Heidelberg. https://doi.org/10.1007/978-3-642-00475-9_18

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free