Lung Cancer. 2007;55(3):279-86.
Adenovirus expressing shRNA to IGF-1R enhances the chemosensitivity of lung cancer cell lines by blocking IGF-1 pathway.
제1저자 이윤진 · 교신저자 이춘택
소속 (1)
- Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine and Lung Institute of Medical Research Center, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Abstract
RNA interference is a phenomenon whereby small double-stranded RNA knocks down the expression of a sequence-specific gene. Double-stranded siRNA transfection, as currently used, is considered to have transient and low transfection efficiency. We constructed an adenoviral vector-based short hair-pin(sh)RNA system to overcome the limitations of the genetic blockade of IGF-1R, one of most important cancer therapy targets. We constructed three different IGF-1R specific shRNAs (612, 801, and 3425) and generated three ad-shIGF-1Rs using BD Adeno-X expression system. We assessed the effect of ad-shIGF-1R on signal transduction, induction of apoptosis, and in vitro tumorigenicity of lung cancer cell lines. Western blot and FACS assays demonstrated that endogenous IGF-1R expression was efficiently suppressed after transduction of lung cancer cell lines with the three different ad-shIGF-1Rs. IGF-1R blockade by ad-shIGF-1R inhibited ligand induced phosphorylation of pAkt and pErk, and ad-shIGF-1R effectively blocked the in vitro tumorigenicity of lung cancer cell lines. Moreover, the transduction of a human lung cancer cell line with ad-IGF-1R(3425) enhanced chemosensitivity to anticancer drugs. We conclude that the adenoviral vector-based approach to the RNA interference of IGF-1R induced effective IGF-1R silencing in lung cancer cell lines as manifested by effective blocking of the downstream pathway of IGF-1R and by an antitumor effect. We believe that this system can be usefully applied to other cancer targets.
그 밖의 정보
- 출판 형태
- Journal Article
- 저널
- Lung cancer (Amsterdam, Netherlands) · ISSN 0169-5002
- 전자 출판
- 2006-11-28
- MeSH
- Adenoviridae / genetics · Antineoplastic Agents / therapeutic use · Apoptosis · Base Sequence · Caspase 3 / drug effects / metabolism · Cell Line, Tumor · Genetic Therapy / methods · Humans · Lung Neoplasms / drug therapy / genetics / metabolism · Molecular Sequence Data · Phosphorylation · RNA Interference* · RNA, Messenger / metabolism · RNA, Small Interfering / pharmacology · RNA, Viral / metabolism · Receptor, IGF Type 1 / antagonists & inhibitors / metabolism · Signal Transduction / physiology · Transduction, Genetic
- Substances
- Antineoplastic Agents · RNA, Messenger · RNA, Small Interfering · RNA, Viral · Receptor, IGF Type 1 · Caspase 3