Silencing insulin-like growth factor-1 receptor expression inhibits gastric cancer cell proliferation and invasion

Mol Med Rep. 2015 Jan;11(1):633-8. doi: 10.3892/mmr.2014.2746. Epub 2014 Oct 22.

Abstract

The oncoprotein insulin-like growth factor-1 receptor (IGF-1R) has previously been shown to promote tumorigenesis. Overexpression of IGF-1R is considered to be a critical prerequisite for malignant transformation in numerous human cancers. Therefore, targeting IGF-1R for cancer therapy has gained a lot of interest. In the present study, an RNA interference (RNAi)-mediated IGF-1R gene silencing approach was conducted in BGC823 gastric cancer cells. The tumorigenic and malignant properties of the cells were assessed, in response to reduced IGF-1R expression. Notably, IGF-1R depletion not only inhibited gastric cancer cell growth, resulted in G1 cell cycle arrest and consequently led to apoptosis, but also suppressed cancer cell motility and invasion. The findings of the present study are the first, to the best of our knowledge, to suggest that RNAi-based IGF-1R silencing may be a potential and promising therapeutic strategy for gastric cancer treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation
  • G1 Phase Cell Cycle Checkpoints / genetics
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing*
  • Humans
  • Neoplasm Invasiveness
  • RNA Interference
  • Receptor, IGF Type 1 / genetics*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / pathology

Substances

  • Receptor, IGF Type 1