Ask about this productRelated genes to: SLC38A5 antibody
- Gene:
- SLC38A5 NIH gene
- Name:
- solute carrier family 38 member 5
- Previous symbol:
- -
- Synonyms:
- SN2, JM24
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-25
- Date modifiied:
- 2015-12-08
Related products to: SLC38A5 antibody
Related articles to: SLC38A5 antibody
- Multiple myeloma (MM) is a glutamine (Gln)-auxotroph and Gln-addicted cancer, with Gln synthetase (GS)-deficient MM cells avidly taking up extracellular Gln to sustain their metabolism. Thus, MM cells create a peculiar metabolic niche in the patients' bone marrow (BM), where low levels of Gln contribute to the osteolytic bone lesions by inhibiting the osteoblastic differentiation of mesenchymal stromal cells (MSCs). The effects of the altered MM metabolic niche on other BM cell populations remain to be clarified. We demonstrate here that MM cells secrete high amounts of glutamate through the exchange transporter /xCT. In turn, BM MSCs, but neither MM cells nor osteoblasts (OBs), actively take up extracellular glutamate through the transporter EAAT3 (), whose expression decreases during osteogenesis. GS-positive MSCs secrete Gln, a process boosted by extracellular glutamate in undifferentiated MSCs, but not in differentiated OBs. Coculture of MSCs with MM cells promotes the expression of the bidirectional transporter SNAT5 (), suggesting its involvement in Gln efflux. Consistently, MSCs, derived from either patients with MM or healthy donors, sustain MM growth in a low-Gln environment, an effect suppressed by the inhibition or silencing of glutamate uptake or Gln synthesis. In conclusion, a metabolic cycle occurs in MM BM microenvironment, where Gln-auxotroph MM cells extrude glutamate that is converted into Gln by MSC, sustaining in turn MM anabolism through Gln secretion. The inhibition of this metabolic trade-off impairs MM cell growth, thus highlighting novel potential, niche-oriented therapeutic targets. - Source: PubMed
Publication date: 2026/01/14
Taurino GiuseppeGriffini ErikaToscani DeniseMaccari ChiaraTardito SaverioBianchi Massimiliano GCasati LaviniaDander EricaD'Amico GiovannaAndreoli RobertaGiuliani NicolaBussolati OvidioChiu Martina - The tumor microenvironment of oral squamous cell carcinoma (OSCC) is shaped by complex metabolite-mediated cell-cell communication (mCCC), the functional role of which remains incompletely understood. This study aimed to identify key mCCC pathways in OSCC and elucidate the mechanisms by which tumor cells respond to these metabolic signals. - Source: PubMed
Publication date: 2026/02/19
Liu YuanhangGuo JieXu HuiXu XiaoxueJin XinxinZhang YahongQiu Yongle - Colorectal cancer (CRC), a malignancy characterized by high aggressiveness, metastatic propensity, frequent recurrence, and poor prognosis, underscores the critical need for identifying biomarkers to guide targeted therapeutic strategies. Solute carrier family 38 member 5 (SLC38A5) emerges as a promising target due to its pharmacological tractability and role in cancer progression. In this study, we demonstrate that SLC38A5 promoted CRC progression through both bioinformatic analysis and experimental validation. Knockdown of SLC38A5 significantly suppressed cell viability, colony formation, and migratory ability in DLD1 and HCT116 cells. Notably, SLC38A5 depletion sensitized CRC cells to RSL3-induced ferroptosis. Mechanistically, SLC38A5 inhibition down-regulated antioxidant-related genes Nrf2 and Heme Oxygenase 1 (HO-1) and key ferroptosis regulators GPX4 and SLC7A11, while modulating Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4) and Stearoyl-CoA Desaturase 1 (SCD1) expression. Additionally, SLC38A5 knockdown impaired nuclear translocation of YAP, the core transcriptional co-activator in the Hippo signaling pathway. Chromatin immunoprecipitation (ChIP) analysis demonstrated the binding of YAP to Nrf2. Our findings reveal a novel mechanism wherein SLC38A5 confers ferroptosis resistance in CRC via YAP nuclear translocation within the Hippo signaling pathway. Collectively, this study highlights SLC38A5 as a potential therapeutic target to enhance ferroptosis-based cancer therapy, offering new strategies to improve CRC treatment outcomes. - Source: PubMed
Publication date: 2025/12/16
Zhang XingZhang JiaqiPeng HaifengLiu XiaofanZhang Hongsheng - Studies show that coenzyme Q10 (CoQ10) has multiple benefits for improving idiopathic male infertility. However, its protective effects against hypoxia-induced damage to the male reproductive system and varicocoele-associated spermatogenesis dysfunction need further investigation. - Source: PubMed
Publication date: 2025/10/07
Chen XinLiu WenjingShi JingtianChen ZhaoyuHan MingliangJiang HuiZhang XianshengWan YangyangHua Juan - Cadherin 17 (CDH17) plays a crucial role in the metastatic progression of colorectal cancer (CRC) through its interaction with α2β1 integrin and desmocollin 1. To further elucidate the molecular mechanisms involving CDH17 functions in CRC, we examined global expression alterations following CDH17 silencing in various metastatic cell lines. Loss of CDH17 resulted in a marked down-regulation of the intestinal cancer stem cell (CSC) marker LGR5, leading to the inhibition of Wnt/β-catenin signaling, suppression of pluripotency genes such as MYC, and a subsequent reduction in stemness properties. Treatment with CDH17/integrin blocking antibodies produced similar effects, decreasing both, LGR5 expression and Wnt signaling. CDH17 silencing also down-regulated various transporters associated with drug-resistance, including the glutamine-transporter SLC38A5. Consequently, the loss of CDH17 increased sensitivity to 5-FU, irinotecan, oxidative stress and anoikis in CRC cells. Notably, SLC38A5 silencing was necessary for CDH17-driven effects on drug resistance and survival. Pharmacological inhibition of SLC38A5 with amiloride, significantly increased cell sensitivity to 5-FU and irinotecan, and improved mouse survival in metastasis models. In conclusion, CDH17 plays a crucial role in maintaining colorectal cancer cell stemness and chemoresistance via LGR5/Wnt/MYC signaling and SLC38A5 expression. These findings underscore the therapeutic potential of CDH17 targeting in metastatic CRC, and support the use of amiloride for inhibiting liver metastasis. - Source: PubMed
Publication date: 2025/07/01
Bartolomé Ruben APintado-Berninches LauraRobles JavierCalvo-López TaniaBoukich IssamOtero-Núñez PabloGonzalez-Sancho Jose ManuelCasal J Ignacio