{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC2A5, which encodes the fructose‐specific transporter GLUT5, functions primarily to mediate the cellular uptake of fructose from dietary and circulating sources. Its expression is tightly regulated in a tissue‐ and context‐dependent manner. In human intestinal and muscle cells, as well as in certain leukocyte subsets, fructose exposure—as well as related signaling effectors such as cAMP and glucocorticoids—modulate both the transcription and the stability of SLC2A5 mRNA, thereby fine‐tuning fructose absorption and utilization. In intestinal epithelial models, fructose and even glucose elevate GLUT5 promoter activity and mRNA half‐life via cAMP‐dependent pathways, while in leukocytes and muscle fibers, its expression is linked to cellular metabolic demands and fiber type specificity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its physiological role in fructose handling, SLC2A5 is frequently upregulated in a number of cancers and malignancies, thereby contributing to tumor metabolism, progression, and therapeutic resistance. In lung cancer cells, GLUT5 facilitates the incorporation of dietary fructose into lipogenic pathways that support rapid cell proliferation and survival via mTORC1 signaling, while in prostate and colorectal cancers, differences in GLUT5 distribution hint at alternative metabolic substrate usages under hypoxic or low‐glucose conditions. Alterations in SLC2A5 expression have also been linked to chemoresistance in colon cancer and in pediatric leukemias, where oncogenic signals (for example, driven by BCR‐ABL1 or via deregulated microRNAs) promote fructose uptake and metabolic reprogramming. Additionally, aberrant expression patterns in renal cell carcinomas and gliomas further underscore its role in sustaining malignant phenotypes across a spectrum of tumors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, emerging evidence links altered GLUT5 function to metabolic diseases and highlights its therapeutic potential. In conditions ranging from fructose malabsorption and obesity‐related disorders to diabetic complications, modulation of SLC2A5 expression has been proposed as a means to correct aberrant fructose metabolism. Serum levels of GLUT5 and genetic variations in SLC2A5 have been correlated with disease severity and could serve as biomarkers, while pharmacologic targeting of GLUT5—a strategy that has shown promise in preclinical cancer models—may offer novel avenues to curb tumor growth or alleviate nutrient absorptive defects associated with high‐fructose dietary intake."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Florence Gouyon, Cercina Onesto, Veronique Dalet, et al. 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