Inhibition of apoptosis by amphiregulin via an insulin-like growth factor-1 receptor-dependent pathway in non-small cell lung cancer cell lines.

The reciprocal activation of amphiregulin (AR) and insulin-like growth factor-1 (IGF1) pathways has been shown to induce inhibition of serum deprivation apoptosis in non-small cell lung cancer (NSCLC) cell lines H358 and H322. We demonstrated that AR activated the IGF1 receptor (IGF1-R), which in turn induced the secretion of AR and IGF1. Transactivation of the IGF1-R by AR is independent of its binding to EGFR. Thus, AR can inhibit apoptosis in NSCLC cells through an IGF1-R-dependent pathway.