Ask about this productRelated genes to: SLC13A2 antibody
- Gene:
- SLC13A2 NIH gene
- Name:
- solute carrier family 13 member 2
- Previous symbol:
- -
- Synonyms:
- NaDC-1
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-26
- Date modifiied:
- 2016-10-05
Related products to: SLC13A2 antibody
Related articles to: SLC13A2 antibody
- Metabolic reprogramming is a hallmark of cancer, while tricarboxylic acid cycle is increasingly recognized as a multifaceted hub driving tumor metabolism and progression. Integrated analysis of solute carrier (SLC) transporters revealed consistent down-regulation of SLC13A2 in hepatocellular carcinoma (HCC) cells and liver tissues from human patients and mouse models. Adeno-associated virus-mediated liver-specific knockout or overexpression of SLC13A2 (SLC13A2-OE) promoted or ameliorated HCC progression, indicating its protective role. SLC13A2 inhibited HCC proliferation by decreasing mitochondrial function via suppressed glycolysis, respiration, and adenosine 5'-triphosphate production. Flux analysis showed that SLC13A2 imported citrate to generate acetyl-coenzyme A for pyruvate kinase isozyme type M2 acetylation, triggering its degradation. Reduced pyruvate kinase activity limited pyruvate supply, impairing amino acid synthesis and nucleotide metabolism. Moreover, SLC13A2-imported citrate induced intracellular protein acetylation, particularly histone proteins, which provided an epigenetic basis for transcriptional regulation and contributed to tumor suppression. Thus, SLC13A2 perturbs metabolic and transcriptional programs to suppress tumor growth, highlighting potential drug targets for HCC therapy. - Source: PubMed
Publication date: 2026/04/08
Qin MengyaoShang LongchengChen HaoShi LiLiu ChanDing MingHe DandanShao ChangYuan ShengtaoYu HongHao HaipingMa YongXiong Jing - The SLC13 gene family encodes plasma membrane transporters with 11 putative transmembrane domains and comprises two functional subgroups: sodium-sulfate cotransporters (NaS) and sodium-carboxylate cotransporters (NaC). The NaC subfamily includes the low-affinity sodium-dicarboxylate cotransporter 1 (NaDC1/SLC13A2), the high-affinity sodium-dicarboxylate cotransporter 3 (NaDC3/SLC13A3) and the sodium-dependent citrate transporter (NaCT/SLC13A5), which facilitate the cellular uptake of tricarboxylic acid cycle (TCA) intermediates such as citrate, succinate and α-ketoglutarate. These substrates serve dual roles as metabolic fuels and signaling molecules. This review synthesizes recent advances in the structural biology, substrate specificity, tissue distribution, and regulation of NaC transporters, and highlights their emerging pathophysiological significance. Dysregulation of NaC transporters contributes to various human diseases, including metabolic disorders (e.g., nephrolithiasis and fatty liver disease), neurological conditions, and cancer. Elucidating the molecular mechanisms governing the function of NaC transporters is crucial for understanding disease etiology and developing targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/01/23
Li PingChen BinxinDong MinleiLuo JunLin NengmingLi Yangling - The aryl hydrocarbon receptor (AHR) is a xenosensor that mediates the toxic effects of exposure to environmental contaminants, such as polycyclic and halogenated aromatic hydrocarbons. Besides its role in metabolism, the AHR is involved in several physiological and pathological processes, such as cell proliferation and tumorigenesis. In particular, the activation of the AHR is associated with greater susceptibility to cervical cancer development, and several AHR-driven gene signatures correlate with cervical cancer survival. However, many aspects of the processes and factors that determine AHR activation and cell localization during tumorigenesis remain unclear. The aim of the present study was to identify the mechanisms involved in the regulation of the cell density-dependent localization of the AHR in HeLa cells. The results show that the low cell density-dependent nuclear localization of the AHR is driven by the availability of tryptophan, an essential source of AHR ligands such as kynurenine. They also indicate that c-MYC expression is promoted at low cell density, mediating the induction of SLC1A5 and SLC3A2, genes encoding for solute carriers involved in tryptophan transport and cell uptake. Moreover, our data also establish that under low cell density conditions SLC1A5, SLC3A2, and AHR expression are under β-catenin and c-MYC control. As β-catenin promotes c-MYC gene induction, the current data allow us to propose that once cell-cell interaction is lost, the release of β-catenin from its interaction with cadherin triggers AHR activation and nuclear internalization. - Source: PubMed
Publication date: 2025/12/17
Flores-Pérez AlegreMurillo-González Fátima EHernández-Toledano David SebastiánLimón-Pacheco Jorge HCabildo-Delgado ItzelVega LibiaElizondo Guillermo - Colorectal cancer (CRC) is a major cause of cancer-related death, with a poor prognosis often due to metastasis and recurrence. Dietary restriction (DR) is known to delay tumor progression and extend lifespan, but the roles of dietary restriction-responsive genes (DRRGs) in CRC remain unclear. This study aimed to identify prognostic DRRGs and explore their associations with tumor behavior and immune features. - Source: PubMed
Publication date: 2025/11/26
Li QibinWang ZengtaoLong JinyiXu ZiyangZhang Jie - Colorectal cancer is a highly lethal gastrointestinal tract malignancy whose pathogenesis and molecular drivers are not fully understood. This study focused on searching for genes that are differentially expressed in cancer versus normal mucosa, with the goal of identifying molecular patterns of expression that are mechanistically linked to colorectal cancer pathogenesis. We analyzed 585 colorectal cancer samples and 329 normal samples from the Gene Expression Omnibus database, creating a weighted gene coexpression network analysis across 24,069 genes. Through this approach, five modules associated with colorectal cancer were identified, which were enriched in MAPK signaling and cholesterol metabolism pathways. Using least absolute shrinkage and selection operator (LASSO) regression, we selected 13 hub genes [ABCB5, AOC1, ARHGAP44, CACNG3, dysbindin domain-containing protein 1 (DBNDD1), GAS7, GTF2IRD1, PRSS22, SCN4A, TTC22, DLX6, PDK4, and SLC13A2] from these modules. Survival analysis indicated that higher expression of DBNDD1 correlated with worse overall survival in patients with colorectal cancer. Machine learning validation confirmed the stability of these genetic markers. Experimental validation demonstrated increased levels of DBNDD1 and growth differentiation factor 15 (GDF15) in colorectal cancer, promoting constant NF-κB (RELA) activation via DBNDD1-dependent GDF15 induction. Knocking down DBNDD1 inhibited cell proliferation, migration, and invasion in vitro (DLD1/HCT116 cells), alongside decreased GDF15 expression and reduced p-NF-κB p65-p-I-κB signaling. Additionally, DBNDD1 knockdown resulted in reduced tumor growth in vivo, highlighting that the DBNDD1-GDF15-NF-κB signaling pathway drives colorectal cancer pathogenesis. - Source: PubMed
Qi XiaominBai CaijuanDong LiWang AnqiWei ChaojunLi YonghongZhao MengyuanYou Chongge