No abstract

The expression and clinical significance of insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein 3 (IGFBP-3), and insulin-like growth factor binding protein 7 (IGFBP-7) were investigated in serum and lung cancer tissues from 57 patients with non-small cell lung cancer (NSCLC). Lung cancer tissues at different pathologic stages (27 patients at stages I–II and 30 patients at stages III–IV), normal lung tissues from 17 patients with benign pulmonary disease, and serum samples from both lung cancer and benign pulmonary disease patients were collected during surgery. Enzyme-linked immunosorbent assay and avidin-biotin-peroxidase complex immunohistochemical staining were used to detect IGF-1, IGFBP-3, and IGFBP-7 expression in serum and tissues, respectively. The results show that expression of IGF-1 in lung cancer tissues and serum from NSCLC patients were significantly higher than in the control (P < 0.05). However, expression of IGFBP-3 and IGFBP-7 in cancer tissues and serum from NSCLC patients was significantly lower than in the control (P < 0.05). These results suggest that upregulation of IGF-1 and downregulation of IGFBP-3 and IGFBP-7 may be potential diagnostic biomarkers for NSCLC.

Insulin-like growth factor 1 receptor (IGF1R) is a tyrosine kinase receptor implicated in tumourigenesis that may be an attractive target for anti-cancer treatment. In this study, the expression and clinical significance of IGF1R were investigated in serum and lung cancer tissues from small cell lung cancinoma (SCLC). We also compared the effect of IGF1R up-regulation and IGF1R inhibition on viability and apoptosis of NCI-H446 cells. We found the concentration of IGF1R in blood serum was significantly increased and positive IGF1R protein in cancer tissue was more prevalent in SCLC. A statistically significant correlation among IGF1R-positve tumors, lymph node metastasis and local invasion was discussed. Furthermore, IGF1R overexpression lead to an increase of cell survival and suppressed cell apoptosis, IGF1R silencing mediated by RNAi abrogate this response of NCI-H446 cells. Our results further demonstrated that the effects of these treatments may be assigned to the effective inhibition of lung cancer cells from Akt/P27(Kip1) pathway in IGF-1R signaling. These features may have important implications for future anti-IGF1R therapeutic approaches.