Ask about this productRelated genes to: SPHK1 antibody
- Gene:
- SPHK1 NIH gene
- Name:
- sphingosine kinase 1
- Previous symbol:
- -
- Synonyms:
- SPHK
- Chromosome:
- 17q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-01
- Date modifiied:
- 2015-08-26
Related products to: SPHK1 antibody
Related articles to: SPHK1 antibody
- Endometrial cancer (EC) is the most common gynecological malignancy in postmenopausal women. Patients with low estrogen receptor alpha (ERα) expression frequently develop aggressive pathological subtypes and have poor prognosis. The role of estradiol (E2) in ERα-low EC remains poorly understood. This study investigated the tumor-promoting effects of E2 using clinical data, in vitro functional assays, and a mouse xenograft model. We found that serum E2 levels were elevated in ERα-low patients, of whom 67.7% showed high tumor expression of G protein-coupled estrogen receptor (GPER). High GPER expression correlated with increased E2 levels, enhanced sphingosine kinase 1 (SphK1) activity, and higher Ki67 proliferation index. In vitro, E2 promoted proliferation, migration, and invasion of HEC-1A cells (low ERα, high GPER). These effects were suppressed by pharmacological inhibition or siRNA knockdown of GPER or SphK1. Mechanistically, E2 activated the ERK1/2 pathway via the GPER/SphK1 axis, leading to upregulation of Cyclin D1, Cyclin E1, and MMP-9. In vivo, E2 stimulated xenograft tumor growth, an effect mitigated by inhibitors of GPER, SphK1, and ERK. Our findings demonstrate that E2 drives progression of ERα-low endometrial cancer through the GPER/SphK1 signaling pathway, revealing potential therapeutic targets for this high-risk subgroup. - Source: PubMed
Wang XiuwenSun HaofeiWen XinXin WeiweiHu ZhandongZhao ZhongweiZhang Lizhi - This study established a rat model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) to evaluate pathological damage, collagen deposition, inflammatory cytokine levels, and key gene/protein expression following water extract (HDWE) intervention. Combined with ultra-high-performance liquid chromatography-quadrupole Orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS), transcriptomic analysis, and molecular simulation, this study identified the bioactive components of HDWE, evaluated their potential interactions with ALI-related targets, and explored the multi-omics-based protective mechanisms of HDWE. - Source: PubMed
Publication date: 2026/09/04
Lu ChenyiYang XinyiYang Xin - Neutrophils are increasingly recognised as immunosuppressive drivers of hepatocellular carcinoma (HCC), yet their persistence in the oxidative, lipid-rich tumour microenvironment remains poorly understood. - Source: PubMed
Publication date: 2026/09/07
Ma JunWu TongChen DiyuZhu CanHuang ShanheDu KeyiPeng ChuanhuiChen JunruChen YunhaoXie HaiyangZhang FengChen JianzhongZheng ShusenWu Jian - Chronic endometritis (CE) is a persistent inflammatory disorder of the endometrium that is increasingly recognized as an important cause of reproductive failure. However, the molecular mechanisms by which CE impairs endometrial receptivity remain incompletely understood. Here, we found that decidualization markers IGFBP1 and PRL were significantly decreased in CE patients, accompanied by abnormal glandular architecture. Transcriptomic analysis revealed sphingolipid metabolism as a dysregulated pathway, with SphK1 markedly downregulated. S1P levels were reduced in both CE tissues and LPS-treated stromal cells during decidualization. Functional experiments confirmed that SphK1 is essential for this process, and its deficiency impairs decidualization. Mechanistically, transcription factor C/EBPδ directly bound and activated the SphK1 promoter. CE endometrium showed reduced C/EBPδ and SphK1, alongside increased LC3B, indicating autophagic dysregulation. Furthermore, S1P was demonstrated to act extracellularly through the G protein-coupled receptor S1PR3 to maintain autophagic homeostasis, thereby regulating endometrial decidualization. In conclusion, suppression of the C/EBPδ-SphK1 axis impairs decidualization with excessive autophagy, revealing a mechanistic link between chronic inflammation, sphingolipid dysregulation, and reproductive failure. - Source: PubMed
Publication date: 2026/09/07
Xiao JiahuiYu ShuyiXu ShiruYou GuanyingMo MeilanLian RuochunChen CongZhang XuelingLi Yuye - Huangqin Qingre Chubi Capsules(HQC) are commonly used in clinical practice to treat rheumatoid arthritis(RA). It is composed of Scutellariae Radix, Gardeniae Fructus, Coicis Semen, Clematidis Radix et Rhizoma, and the stir-fried Persicae Semen. However, the pharmacological substance basis and mechanism are not yet clear. This study systematically elucidated the pharmacological substance basis and mechanism of HQC by the research strategy of "identification of target tissue migration components-network mechanism prediction-multidimensional experimental verification". An adjuvant-induced arthritis(AA) rat model was established, and the serum and synovium migration components of HQC in normal and AA model rats were analyzed using ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry(UPLC-Q-TOF-MS/MS). These serum and synovium migration components were integrated for network pharmacology prediction, which was followed by multi-dimensional validation using molecular docking, RT-qPCR, and pharmacodynamic evaluation. The results showed that 46 serum and 13 synovium migration components were identified in normal rats, and 59 serum and 15 synovium migration components were identified in AA rats, indicating that the RA disease environment affects the entry of HQC into the bloodstream and migration to the synovium. Comparative analysis of components common and unique to normal and model groups identified geniposide, baicalin, daucosterol, coptisine, acteoside, luteolin, and crocin as migration components reaching the target site, reflecting the target tissue enrichment characteristics of HQC. Network pharmacology of the migration components screened 7 core targets: GAPDH, TNF-α, AKT1, PTGS2, NF-κB1, MAPK1, and SphK1, which were enriched in key RA signaling pathways including PI3K-AKT, HIF-1, VEGF, and TNF. Molecular docking and RT-qPCR confirmed good binding activity and regulatory capacity between key components and core targets. In vivo validation further demonstrated that HQC significantly improved joint inflammation and synovial hyperplasia in AA rats. This study confirmed that HQC exerted an anti-RA effect by targeting chronic inflammation and metabolic disorders through multi-target regulation of PI3K-Akt and other signaling pathways via serum and synovium migration components. The research provides a scientific basis for the clinical application of HQC and offers a new strategy for studying the mechanisms of TCM. - Source: PubMed
Pang JingGan Pei-RongZhu Yu-LongWang YingBu Yan-HongWu Hong