Knockdown of type I insulin-like growth factor receptor inhibits human colorectal cancer cell growth and downstream PI3K/Akt, WNT/β-catenin signal pathways.

Type I insulin-like growth factor receptor (IGF1R) signal is involved in normal physiology and many disease progressions. In this study, we presented the role of IGF1R in colorectal cancer cell lines. Results showed that knockdown of IGF1R using small interfering RNA in HT-29, SW620 cells strongly inhibited cell proliferation, arrested cell cycle and also promoted cell apoptosis. Western blotting results indicated that the downstream PI3K/Akt and canonical WNT signal pathways were blocked. In addition, we observed that reduction of IGF1R suppressed the expression of many inflammatory factors, such as NF-κB, p-NF-κB, COX-2 and iNOS. Together, this study demonstrate that knockdown of IGF1R inhibits CRC cells growth and provides an additional evidence for further clarifying the mechanism of IGF1R involved in CRC and inflammation-induced tumorigenesis.