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<p>The SLC45 family emerges as a proton-coupled sugar transport system that complements the classical SGLT (SLC5) and GLUT (SLC2) transporters in mammals. This review synthesizes recent advances on four family members (SLC45A1–A4), covering their structural features (12-pass transmembrane topology with a pH-sensing cytoplasmic loop), genomic organization across chromosomes 1p36.1, 5p13.3, 1q32.1, and 8q24.3, and diverse physiological roles in brain glucose homeostasis, melanogenesis, lipid metabolism, and cancer metabolic reprogramming. We highlight disease associations, including SLC45A1 mutations causing epileptic encephalopathy, SLC45A2 variants linked to oculocutaneous albinism and melanoma risk, SLC45A3 fusions driving prostate cancer, and SLC45A4 overexpression in ovarian/pancreatic cancers. Recent literature reveals tissue-specific regulatory mechanisms (e.g., androgen signaling for SLC45A3, TP53-MYC axis for SLC45A4) and therapeutic potential spanning ketogenic diets, gene therapy, peptide vaccines, and siRNA nanoliposomes. We conclude by identifying critical knowledge gaps—such as the lack of mammalian structures and undefined substrate spectra—that must be addressed to translate SLC45 biology into precision medicine.</p>

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Sugar transporter SLC45 gene family members: roles in malignant tumors and research progress

  • 期刊论文

  • 发表日期：

    2026年1月12日

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  • Yuance Xu,
  • Danting Sun,
  • Chao Wang,
  • Qin Yao

摘要

The SLC45 family emerges as a proton-coupled sugar transport system that complements the classical SGLT (SLC5) and GLUT (SLC2) transporters in mammals. This review synthesizes recent advances on four family members (SLC45A1–A4), covering their structural features (12-pass transmembrane topology with a pH-sensing cytoplasmic loop), genomic organization across chromosomes 1p36.1, 5p13.3, 1q32.1, and 8q24.3, and diverse physiological roles in brain glucose homeostasis, melanogenesis, lipid metabolism, and cancer metabolic reprogramming. We highlight disease associations, including SLC45A1 mutations causing epileptic encephalopathy, SLC45A2 variants linked to oculocutaneous albinism and melanoma risk, SLC45A3 fusions driving prostate cancer, and SLC45A4 overexpression in ovarian/pancreatic cancers. Recent literature reveals tissue-specific regulatory mechanisms (e.g., androgen signaling for SLC45A3, TP53-MYC axis for SLC45A4) and therapeutic potential spanning ketogenic diets, gene therapy, peptide vaccines, and siRNA nanoliposomes. We conclude by identifying critical knowledge gaps—such as the lack of mammalian structures and undefined substrate spectra—that must be addressed to translate SLC45 biology into precision medicine.