166 - Effect of Neural Cell Adhesion Molecule Expression on Glycolytic Pathway in Melanoma

Abstract

ABSTRACT Background Neural cell adhesion molecule (NCAM), a member of the immunoglobulin superfamily, has been well characterized in cell-cell adhesion, neurite outgrowth, and synaptic plasticity. Recent studies have also shown that the expression of NCAM affects tumor progression. Indeed, the expression of NCAM has been implicated in the cellular invasion and metastasis of melanoma. Like many other malignant tumors, melanomas are dependent on aerobic glycolysis for ATP production. Many studies have consistently correlated poor prognosis and increased tumor aggressiveness with increased glucose uptake. In this study, we tested whether the expression of NCAM influences glycolytic pathways in mouse melanoma cell line. Methods We constructed a recombinant viral vector derived from adeno-associated virus serotype 2 (rAAV2) that expresses NCAM. Mouse melanoma cell line B16F10 was transduced with rAAV2. We performed in vitro fluorine-18 fluorodeoxyglucose (18F-FDG) uptake assay in a gamma counter. In addition, western blot analysis was carried out for glucose transporters (GLUT) and hexokinases (HK). Results Transduction of B16F10 cells with rAAV2 NCAM resulted in increased 18F-FDG uptake. Western blot analyses demonstrated that the 180-kDa isoform of NCAM (NCAM 180) was up-regulated. Expression levels of GLUT1, GLUT2 and HK II were elevated. Conclusions Overexpression of NCAM was associated with elevated levels of GLUT1, GLUT2, and HK II, which contributes to increased glycolysis. We demonstrated that 18F-FDG uptake might be used as a surrogate marker for assessing NCAM expression in melanoma. In terms of monitoring NCAM expression, the utility of 18F-FDG uptake as a prognostic indicator requires further elucidation. Disclosure All authors have declared no conflicts of interest.