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The metabolism of cancer cells is highly plastic. Cancer cells can change their preference for nutrient uptake under nutrient stress. Fructose is one of the most common carbohydrates in diet and its metabolism is also involved in the development and progression of tumors. GLUT5, encoded by  SLC2A5 , is the specific fructose transporter in mammalian cells. In this study, we found that  SLC2A5  is significantly upregulated in lung adenocarcinoma (LUAD) patients and overexpression of  SLC2A5  is highly correlated with poor prognosis of LUAD patients. The expression of  SLC2A5  determined fructose uptake and utilization efficacy in LUAD cells. GLUT5 is critical for the survival of LUAD cells in fructose-containing culture medium. Depletion of  SLC2A5  undermined cell proliferation and invasion meanwhile increased cell apoptosis. Overexpression of  SLC2A5  enhances cell proliferation, migration, invasion, and tumorigenic. Compared to glucose, fructose is prone to strengthen intracellular-free fatty acid accumulation and ATP production. Moreover, inhibition of GLUT5 by specific small chemical inhibitor sensitizes LUAD cells to paclitaxel treatment. Taken together, our results suggest that GLUT5 could be a potential target alone or combination with other treatment for lung cancer therapy.

SLC2A5 promotes lung adenocarcinoma cell growth and metastasis by enhancing fructose utilization