Adenovirus expressing shRNA to IGF-1R enhances the chemosensitivity of lung cancer cell lines by blocking IGF-1 pathway

Lung Cancer. 2007 Mar;55(3):279-86. doi: 10.1016/j.lungcan.2006.10.020. Epub 2006 Nov 28.

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.

MeSH terms

  • Adenoviridae / genetics*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis
  • Base Sequence
  • Caspase 3 / drug effects
  • Caspase 3 / metabolism
  • Cell Line, Tumor
  • Genetic Therapy / methods
  • Humans
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • Molecular Sequence Data
  • Phosphorylation
  • RNA Interference*
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / pharmacology*
  • RNA, Viral / metabolism
  • Receptor, IGF Type 1 / antagonists & inhibitors*
  • Receptor, IGF Type 1 / metabolism
  • Signal Transduction / physiology
  • Transduction, Genetic

Substances

  • Antineoplastic Agents
  • RNA, Messenger
  • RNA, Small Interfering
  • RNA, Viral
  • Receptor, IGF Type 1
  • Caspase 3