Ask about this productRelated genes to: SFXN1 antibody
- Gene:
- SFXN1 NIH gene
- Name:
- sideroflexin 1
- Previous symbol:
- -
- Synonyms:
- FLJ12876, SLC56A1
- Chromosome:
- 5q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-25
- Date modifiied:
- 2017-11-24
Related products to: SFXN1 antibody
Related articles to: SFXN1 antibody
- Sideroflexin 1 (SFXN1), predominantly localized in the inner mitochondrial membrane, exhibits differential expression across various tumor types. However, its specific role in colon adenocarcinoma (COAD) remains unclear. This study aimed to investigate the diagnostic and prognostic significance of SFXN1 in COAD. The expression and prognostic value of SFXN1 in COAD were evaluated using the Cancer Genome Atlas (TCGA) database. Bioinformatics analyses were conducted to assess the relationships between SFXN1 expression and clinical stage, prognosis, and immune infiltration in COAD. The biological role of SFXN1 in COAD was further validated through in vivo and in vitro experiments. SFXN1 was found to be expressed at low levels in COAD. Reduced SFXN1 expression was significantly associated with poor clinical outcomes in COAD patients. Furthermore, SFXN1 expression correlated with immune infiltration and immune checkpoint regulation in COAD. Functional experiments demonstrated that SFXN1 inhibition enhanced the proliferation, migration, and invasion of COAD cells, whereas SFXN1 overexpression suppressed tumor growth in vivo. Low SFXN1 expression is associated with an unfavorable clinical prognosis in COAD. Targeting SFXN1 may offer a promising avenue for developing personalized and more effective therapeutic strategies for patients with COAD. - Source: PubMed
Zhu JieHuang YuchenWu XiaoqinZhu LiusuyuLiu JiahaoWei JinhuanSha Xilin - Selenium (Se) is an essential trace element for maintaining cardiovascular health. Although Se deficiency is associated with various vascular diseases, its precise role in venous endothelial injury remains unclear. Therefore, we established the porcine model of Se deficiency in vivo and used SUVECs in vitro to investigate the potential mechanisms of Se deficiency-induced venous inflammatory injury. The results demonstrated that Se deficiency activated ferritinophagy in porcine vein, accompanied by lipid peroxidation and mitochondrial dynamics disorder, ultimately leading to ferroptosis and the release of pro-inflammatory cytokines. In vitro experiments demonstrated that pharmacological inhibition of autophagy or nuclear receptor coactivator 4 (NCOA4) knockout reduced intracellular iron levels and attenuated ferroptosis, suggesting that NCOA4-mediated ferritinophagy was essential for the ferroptosis induced by Se deficiency. Furthermore, Se deficiency upregulated the expression of sideroflexin-1 (SFXN1) in porcine vein. We further found that NCOA4 knockout or treatment with the iron chelator deferoxamine (DFO) markedly downregulated Se deficiency-induced SFXN1 expression, indicating that Fe²⁺ released from NCOA4-mediated ferritinophagy activates SFXN1. What's more, SFXN1 knockout alleviated mitochondrial iron overload, decreased mitochondrial reactive oxygen species (mtROS) and lipid peroxidation, and inhibited ferroptosis. Notably, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) effectively alleviated Se deficiency-induced porcine phlebitis, thereby linking ferroptosis to vascular inflammation. In addition, AMPK-mTOR pathway plays a pivotal role in orchestrating Se deficiency-induced ferritinophagy and subsequent ferroptosis. Overall, these findings elucidate novel mechanisms by which Se deficiency induces venous endothelial injury, and identify ferritinophagy and SFXN1-mediated mitochondrial iron transport as potential therapeutic targets for cardiovascular pathologies associated with Se deficiency. - Source: PubMed
Publication date: 2026/02/12
Qiu YaningXie RuiruiBi GuodongWang QianChu JiahongXu ShiwenLi Shu - Lienal peptides (LPs), one kind of animal-derived traditional Chinese medicine, are used clinically as an adjunctive therapeutic drug in oncology. Cisplatin (DDP) is a broad-spectrum chemotherapy drug widely used for non-small cell lung cancer (NSCLC) but is limited by a series of toxic side effects. To date, the feasibility of using LPs and DDP in combination remains unclear. The present study aimed to explore the feasibility of LPs combined with DDP as an adjuvant therapy for NSCLC by examining the effects of LPs on the efficacy and toxicity of DDP. Our findings demonstrated that LPs exhibited significant antitumor activity in Lewis lung carcinoma (LLC)-bearing mice when administered either alone or combined with DDP. Moreover, LPs treatment notably improved survival rate, alleviated renal and hepatic impairment, and reversed DDP-induced metabolic disorder. Additionally, our data indicated that tumor growth led to dysregulated serine metabolism. LPs could significantly normalize serine levels by modulaitng the synthesis of serine in gut microbiota and its SFXN1-mediated transport in tumor cells. Thus, this study for the first time reveals the auxiliary anti-tumor effect of LPs from the perspective of amino acid metabolism, supporting LPs as a promising adjuvant to DDP in NSCLC. - Source: PubMed
Publication date: 2026/01/16
Ding KeYu TengjieZhang XiaoweiHu KangruiMao ShuyingZhang TingtingLiu YeWang ZhongboFan XinLiu WeiZhang DianzhuiHe LaipengXie LinWang GuangjiLiang Yan - Oral squamous cell carcinoma (OSCC) is a predominant malignancy characterized by aggressive progression and poor prognosis. This study investigated the role of SFXN1 (Sideroflexin 1), a mitochondrial serine transporter, in OSCC using integrated bioinformatic and experimental approaches. - Source: PubMed
Publication date: 2025/11/25
Manickam Natarajan PrabhuKaruppan Perumal Manoj KumarRama Varma SudhirThomas SamOdeh RubaRajan Renuka Remya - Mitochondria are essential organelles involved in energy production, cellular metabolism, and signal transduction. They have important impacts on tumorigenesis and cancer progression. Nevertheless, the associations between mitochondrial metabolic processes and chemotherapy resistance in colorectal cancer (CRC) are not well understood. - Source: PubMed
Publication date: 2025/11/10
Chen ShiyiLi QianZheng Wei