Ask about this productRelated genes to: SLC6A14 Blocking Peptide
- Gene:
- SLC6A14 NIH gene
- Name:
- solute carrier family 6 member 14
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-02-17
Related products to: SLC6A14 Blocking Peptide
Related articles to: SLC6A14 Blocking Peptide
- Solute carrier family 6 member 14 (SLC6A14/ATB) is a broad-spectrum, Na/Cl-dependent amino acid transporter. It mediates the active uptake of nearly all essential amino acids and serves as a critical metabolic hub under physiological and pathological conditions. To fully understand its potential as a therapeutic target for cancer intervention, this review systematically elucidates the structural biology, regulatory networks, and multifaceted roles of SLC6A14 in cancer. By examining the expression patterns of SLC6A14 in physiological and pathological situation, we demonstrate that it's significantly upregulated in various "amino acid-dependent" malignancies. It includes pancreatic cancer, colorectal cancer, and estrogen receptor-positive breast cancer, where it drives multiple signaling pathways and promotes tumor progression through diverse mechanisms. Beyond its classical metabolic functions, SLC6A14-mediated nutrient deprivation establishes a "nutrient-based immune evasion" mechanism, elucidating its potential for intervention in tumor immunity. Furthermore, we outline a dual-pronged therapeutic strategy for SLC6A14, including its use as a target for pharmacological inhibition and as a delivery channel for amino acid-conjugated prodrugs. Finally, we emphasize that successful clinical translation requires a shift from biomarker-driven patient stratification to mechanism-driven implementation. This highlights the central role of SLC6A14 as an intervenable target at the intersection of cancer metabolism, immune regulation, and targeted therapy. - Source: PubMed
Publication date: 2026/06/20
Zang WenchongZhang ZhentaoZhi YeZhang WenSong FeifengHuang Ping - To characterize the amino acid metabolic remodeling in THBEc1 cells malignantly transformed by benzo[a]pyrene (BaP) relative to parental human bronchial epithelial HBE cells, and to delineate the role of FOXA1 in this remodeling, the amino acid metabolic phenotypes and gene expression patterns of HBE, THBEc1, THBEc1-ctrl (knockout control), and THBEc1-FOXA1 KO (FOXA1 knockout) cells were profiled under 2D, 3D spheroid, and in vivo conditions. Differential metabolic amino acids across these growth modes were identified. THBEc1 cells exhibited a glutamine/glutamate/aspartate metabolic shift and urea cycle remodeling that were conserved across all growth modes, representing key metabolic features of BaP-induced malignant transformation. FOXA1 knockout partially reversed these metabolic alterations across growth modes. Mechanistically, FOXA1 transcriptionally regulated GLUL, SLC6A14, CPS1, and SLC7A2 in a growth-mode-independent manner. These findings establish FOXA1 as a key mediator of the glutamine/glutamate/aspartate metabolic shift and urea cycle remodeling during BaP-induced malignant transformation, with GLUL, SLC6A14, CPS1, and SLC7A2 as critical downstream targets. This work advances the understanding of amino acid metabolic reprogramming in BaP-induced lung carcinogenesis. - Source: PubMed
Publication date: 2026/06/16
Fu YujinQi YanminXing YunkunLin YitongLiu ZhiyuFu JuanlingYao BiyunZhao Peng - Inflammatory bowel disease (IBD) is characterized by a refractory, relapsing inflammatory state driven by a multifaceted and poorly understood interplay between host mucosal metabolic disturbances and immune microenvironment dysregulation. To uncover robust non-invasive diagnostic indicators, this study implemented an integrated analytical framework combining advanced machine learning feature selection, penalized logistic regression modeling, and leave-one-dataset-out cross-validation to construct a novel diagnostic signature derived from metabolic cell death-related genes (MCDRGs). Systematic multiple-testing correction and rigorous data harmonization were applied across all independent discovery and validation cohorts to control for potential batch effects. Through this approach, we successfully identified a core three-gene candidate panel comprising indoleamine 2,3-dioxygenase 1 (IDO1), lipocalin 2 (LCN2), and solute carrier family 6 member 14 (SLC6A14). Methodologically, we demonstrated that the initial near-perfect apparent discrimination within the discovery cohort was mathematically attributable to quasi-complete data separation rather than systemic model overfitting. This identified signature exhibited consistent cross-cohort validation and correlated tightly with the coordinated infiltration and functional states of multiple mucosal immune cell subsets. Furthermore, independent clinical assays substantiated the synchronized elevation of these markers during active clinical phases, while orthogonal single-cell RNA-sequencing confirmed their prominent, cell-type-specific enrichment within the myeloid, epithelial, and stromal compartments of inflamed intestinal mucosa. Collectively, the identified MCDRGs, IDO1, LCN2, and SLC6A14, link metabolic dysregulation, immune infiltration, and regulated cell death, offering insights into IBD pathophysiology and providing a transcriptomic candidate signature with exploratory diagnostic potential for IBD stratification. - Source: PubMed
Publication date: 2026/06/15
Xu FengminHe ZhentingLi QianqianChen Yuling - Hepatocellular carcinoma (HCC) remains a major malignancy with high incidence and mortality, in part due to its diverse etiology and intratumoral heterogeneity, which contributes to drug resistance and frequent recurrence. SALL1 (Spalt-Like Transcription Factor 1), a zinc-finger transcription factor, was reported to function as a tumor suppressor in several cancers, including breast cancer and glioma, and accumulating evidence support its involvement in tumor biology. In this study, the role of SALL1 in HCC was examined. - Source: PubMed
Publication date: 2026/04/24
Saito YoshifumiKasano-Camones Carlos IchiroTamura AtsumiKimura ShiokoYu XiaotingCui YutongSawaswong VorthonKrausz Kristopher WWang DongQu AijuanInoue YusukeTakahashi ShogoGonzalez Frank J - PDAC is highly desmoplastic and undergoes metabolic reprogramming to sustain their growth and proliferation. Our laboratory has identified SLC6A14, an amino acid transporter, as a novel drug target for PDAC. Genetic deletion of SLC6A14 or its pharmacological blockade with α-MLT attenuates PDAC growth by inducing amino acid deprivation. However, nutrient stress, particularly amino acid deprivation, can induce nutrient scavenging mechanisms like autophagy and macropinocytosis, thereby undermining the full anticancer potential of SLC6A14 blockade. To address this, the current work was conducted to test if SLC6A14 blockade induces autophagy and/or macropinocytosis and to further investigate if dual inhibition of SLC6A14 (α-MLT) and autophagy/macropinocytosis (HCQ) would yield a better therapeutic outcome in PDAC as opposed to targeting SLC6A14 alone. In vitro assays (MTT and colony formation) revealed that the combination treatment significantly reduced PDAC cell viability and clonogenic potential as opposed to monotherapy. Treatment model subcutaneous xenograft in athymic nude mice demonstrated a superior therapeutic outcome with the combination regimen. Collectively, our study demonstrates that the afore-described combination therapy creates a metabolic trap wherein α-MLT induces nutrient stress, while HCQ prevents autophagic and macropinocytosis compensation, thus culminating in a more potent tumor attenuation. This dual blockade represents a hitherto unexplored treatment strategy for PDAC. - Source: PubMed
Publication date: 2026/04/08
Bhutia Yangzom DMahmud Syed MosharafRajasekaran DevarajaSennoune Souad RSharker TanimaSanchez OscarJurek Mary KatherineKou LongfaChen RuijieGanapathy Vadivel