Insulin-like growth factor binding protein-2 (IGFBP-2) as a novel biomarker in lung cancer

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Insulin-like growth factors (IGFs) are mitogenic in normal and neoplastic†cells and act by binding to cell-surface IGF receptors. Activation of IGF signaling pathway causes tumorigenesis and tumor progression through the PI3- and MAP-kinase cascades. The IGFs in serum are bound to IGF binding proteins (IGFBPs), which has been shown to regulate the bioavailability of IGFs, in both positive and negative regulatory roles. It has shown IGFBP-2 is overexpressed in a variety of cancers including glioma, prostate, colorectal, ovarian, adrenocortical, breast, and leukemia. Present study demonstrates that IGFBP-2 is a candidate biomarker in lung cancer and suggests its regulatory mechanism. We found that IGFBP-2 was frequently overexpressed in human lung cancer compared to normal tissue, examined by immunohistochemistry (strong, 19%; moderate, 33%; weak, 45%; negative, 3%). Also, we found p-Akt and p-Erk1/2 were overexpressed in lung cancer as it has been previously reported. A comparison among IGFBP-2, p-Akt, p-Erk1/2 expression, and clinicopathological data of 160 patients revealed the positive correlation between IGFBP-2 and p-Akt expression. These data suggest IGFBP-2 is a novel biomarker for PI3K signaling pathway in lung cancer.