{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC1A5 (also known as ASCT2) is a high‐affinity transporter for glutamine that plays a pivotal role in cancer metabolism. In rapidly proliferating tumor cells—including those of triple‐negative breast, prostate, colorectal, melanoma, neuroblastoma, hepatocellular, pancreatic, esophageal, and even acute myeloid leukemia—SLC1A5 sustains the anabolic demands by mediating glutamine uptake that fuels the tricarboxylic acid cycle and activates the mTORC1 nutrient‐sensing pathway. Overexpression of SLC1A5 is often associated with oncogenic drivers (for example, MYCN, ATF4, AR, and STAT3) and its inhibition—either by competitive small molecule antagonists or via genetic knockdown—results in suppressed glutaminolysis, impaired cell cycle progression, increased oxidative stress, and reduced tumor growth and metastasis. These findings together highlight the therapeutic promise of targeting SLC1A5 to overcome drug resistance and enhance tumor sensitivity to oxidative stress and other anticancer therapies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, SLC1A5 function is finely regulated through its structural dynamics and post‐translational modifications. High‐resolution cryo–electron microscopy and kinetic studies have revealed multiple conformational states that underscore the importance of extracellular N‐glycosylation and regulated membrane trafficking for efficient transporter activity. Moreover, when SLC1A5 is lost or inhibited, cancer cells may invoke compensatory mechanisms—up‐regulating alternative transporters such as SNAT1 and SNAT2—to preserve amino acid homeostasis. Together, these studies not only detail the mechanistic basis for glutamine transport but also illustrate how alterations in SLC1A5 regulation can impact both transporter function and downstream metabolic signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in oncogenesis, SLC1A5 is also integral to several physiological processes. It serves as a receptor for retroviral envelope proteins—implicated in syncytialization during placental trophoblast fusion—and is modulated by growth factors such as EGF to enhance nutrient uptake in enterocytes. These functions demonstrate that SLC1A5 not only modulates cellular metabolism but also bridges metabolic regulation with key developmental events and host–virus interactions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Bryan C Fuchs, Richard E Finger, Marie C Onan, et al. 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