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Ganglioside  GD 2 is specifically expressed in small‐cell lung cancer ( SCLC ) cells, leading to enhancement of malignant phenotypes, such as cell proliferation and migration. However, how  GD 2 promotes malignant phenotypes in  SCLC  cells is not well known. In this study, to reveal the mechanisms by which  GD 2 increases malignant phenotypes in  SCLC  cells, we used enzyme‐mediated activation of radical sources combined with mass spectrometry in  GD 2 +   SCLC  cells. Consequently, we identified  ASC  amino acid transporter 2 ( ASCT 2), a major glutamine transporter, which coordinately works with  GD 2. We showed that  ASCT 2 was highly expressed in glycolipid‐enriched microdomain/rafts in  GD 2 +   SCLC  cells, and colocalized with  GD 2 in both proximity ligation assay and immunocytostaining, and bound with  GD 2 in immunoprecipitation/ TLC  immunostaining. Malignant phenotypes of  GD 2 +   SCLC  cells were enhanced by glutamine uptake, and were suppressed by L‐γ‐glutamyl‐p‐nitroanilide, a specific inhibitor of  ASCT 2, through reduced phosphorylation of p70 S6K1 and S6. These results suggested that  ASCT 2 enhances glutamine uptake in glycolipid‐enriched microdomain/rafts in  GD 2 +   SCLC  cells, leading to the enhancement of cell proliferation and migration through increased phosphorylation of the  mTOR  complex 1 signaling axis.

ASC amino acid transporter 2, defined by enzyme‐mediated activation of radical sources, enhances malignancy of GD2‐positive small‐cell lung cancer