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Amino acid transporters are membrane proteins responsible for the uptake of amino acids into cells, a process highly upregulated in tumor cells to support their rapid growth and metabolic demands. Key transporters that support tumor proliferation and survival include SLC1A5 (ASCT2, mainly glutamine uptake), SLC7A5 (LAT1, large neutral amino acids), SLC7A11 (xCT, cystine/glutamate exchange), and SLC43A1 (facilitates import of large neutral essential amino acids). These transporters are often overexpressed or hyperactivated in cancer compared to normal tissues. They play a crucial role in metabolic reprogramming, fueling signaling cascades like mTORC1, and supporting oncogene activity (such as MYC-driven metabolism). Multiple tumor types—including breast, lung, and hematological malignancies—show dependency on these transporters. As a group, amino acid transporters are considered both biomarkers and validated targets for therapeutic intervention, with several inhibitors and monoclonal antibodies under preclinical and clinical investigation. The target term “tumor cells with increased amino acid transporters” is not a canonical name, but refers to a group of transporters; for structured information, mapping to individual well-annotated transporters (e.g., SLC1A5, SLC7A5) is necessary for precision. Notes: - The phrase provided is not a standard molecular target name, but rather a description of a tumor phenotype. The recommendation is to specify the exact transporter(s), such as "SLC1A5 (ASCT2)" or "SLC7A5 (LAT1)", for structured data applications. - The list of aliases and molecular classifications reflects the heterogeneity of transporter upregulation in tumors. - Disease/biomarker/mechanism entries encompass general findings shared among many cancer-associated amino acid transporters, not a single molecule. This approach allows you to map specific tumor-associated amino acid transporters into structured databases for downstream targeting and analysis.
Inhibition of amino acid uptake (starving tumor cells, leading to apoptosis or growth arrest) Antibody-dependent cellular cytotoxicity (for anti-SLC3A2, e.g., IGN523) Indirect modulation of metabolic signaling (e.g., mTORC1 pathway by limiting amino acid supply)
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