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    BIOMARKER:

    SLC7A5 overexpression

    i
    Other names: SLC7A5, Solute Carrier Family 7 Member 5, MPE16, LAT1, E16, Solute Carrier Family 7 (Amino Acid Transporter Light Chain, L System), Member 5, Large Neutral Amino Acids Transporter Small Subunit 1, L-Type Amino Acid Transporter 1, Integral Membrane Protein E16, CD98 Light Chain, 4F2 Light Chain, D16S469E, 4F2LC, CD98, Solute Carrier Family 7 (Cationic Amino Acid Transporter, Y+ System), Member 5, Sodium-Independent Neutral Amino Acid Transporter LAT1, Y+ System Cationic Amino Acid Transporter, CD98LC, 4F2 LC, HLAT1
    Entrez ID:
    8140
    Related biomarkers:
    Expression
    almost2years
    Protein expression of the amino acid transporter SLC7A5 in tumor tissue is prognostic in early-stage colorectal cancer. (PubMed, PLoS One)
    Since SLC7A5 is also a marker of activated lymphocytes such as NK, T, and B lymphocytes, SLC7A5 overexpression in early colorectal cancers might trigger a strong anti-tumor immune response which could results in better clinical outcome. Overall, our study provides clear evidence of differential SLC7A5 expression and its prognostic value for early-stage colorectal cancer, although the understanding of its functions in colorectal tumorigenesis and cancer immunity is currently rather limited and awaits further characterization.
    Journal
    |
    SLC3A2 (Solute Carrier Family 3 Member 2) • SLC7A5 (Solute Carrier Family 7 Member 5)
    |
    SLC7A5 overexpression
    almost2years
    Cancer-associated fibroblasts-derived exosomal METTL3 promotes the proliferation, invasion, stemness and glutaminolysis in non-small cell lung cancer cells by eliciting SLC7A5 m6A modification. (PubMed, Hum Cell)
    In addition, METTL3 inhibition in CAF exosomes impeded NSCLC growth in vivo. In all, CAFs-derived exosomal METTL3 promoted the proliferation, invasion, stemness and glutaminolysis in NSCLC cells by inducing SLC7A5 m6A modification.
    Journal
    |
    SLC7A5 (Solute Carrier Family 7 Member 5) • METTL3 (Methyltransferase Like 3)
    |
    SLC7A5 overexpression
    almost2years
    ALYREF-JunD-SLC7A5 axis promotes pancreatic ductal adenocarcinoma progression through epitranscriptome-metabolism reprogramming and immune evasion. (PubMed, Cell Death Discov)
    In conclusion, this research revealed the relationship between m5C modification, amino acid transportation and immune microenvironment. ALYREF might be a novel target for PDAC metabolic vulnerability and immune surveillance.
    Journal
    |
    CD8 (cluster of differentiation 8) • SLC7A5 (Solute Carrier Family 7 Member 5) • ALYREF (Aly/REF Export Factor)
    |
    SLC7A5 overexpression
    2years
    Treatment outcomes by stratifying the N-acetyl transferase 2 phenotype in pre-treated patients with advanced refractory biliary tract cancer treated with nanvuranlat, an L-type amino acid transporter inhibitor: An ad-hoc analysis of a randomized, double-blind, placebo-controlled phase 2 study. (ASCO-GI 2024)
    By classifying BTC patients by NAT2 phenotype in this ad hoc analysis, the LAT1 inhibitor nanvuranlat further improved its clinical efficacy and safety in the NAT2 NR population. Therefore, selecting NAT2 NR for nanvuranlat treatment may improve the risk -benefit ratio. Clinical trial information: UMIN000034080.
    Clinical • P2 data • Metastases
    |
    SLC7A5 (Solute Carrier Family 7 Member 5)
    |
    SLC7A5 overexpression
    |
    nanvuranlat (JPH203)