Mix EDG-3, CT
- Known as:
- Mix EDG-3, CT
- Catalog number:
- mc-913
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Mix EDG-3
Related genes to: Mix EDG-3, CT
- Gene:
- S1PR3 NIH gene
- Name:
- sphingosine-1-phosphate receptor 3
- Previous symbol:
- EDG3
- Synonyms:
- EDG-3
- Chromosome:
- 9q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-10-05
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- Women living with HIV face an increased burden of spontaneous preterm birth (sPTB); however, the underlying immunological mechanisms of sPTB and its association with HIV infection are poorly understood. Although the limited earlier literature implicates sphingosine-1-phosphate (S1P), a lysosphingolipid signaling molecule, in reproductive biology, the association of S1P signaling with HIV and sPTB has not been investigated. We examined whether two S1P signaling components, S1P receptors and sphingosine kinases, are expressed in the female reproductive tract and whether levels are associated with HIV status or spontaneous preterm birth. We quantified the mRNA expression of sphingosine-1-phosphate receptors 1 and 3 (/) and sphingosine kinases 1 and 2 (/) in 167 banked vaginal swab specimens collected between 14 and 26 weeks of gestation in a longitudinal pregnancy cohort in Lusaka, Zambia. We evaluated the expression of , , , and by real-time quantitative reverse transcription PCR (RT-qPCR) in four groups (n = 41-42 each): women without HIV (WWoH) with term birth (≥37 weeks of gestation; TB), WWoH with spontaneous preterm birth (<37 weeks of gestation, sPTB), women with HIV (WWH) with TB, and WWH with sPTB. We found that S1P receptors and sphingosine kinases are expressed in the female reproductive tract. and mRNA expression were generally comparable among women independent of HIV status or birth outcome, though trended toward higher expression in women with HIV and women with sPTB. In contrast, mRNA trended toward higher expression in WWH vs. WWoH overall, as well as in WWH vs. WWoH among women with sPTB. Similarly, mRNA expression was greater in women with HIV than in women without HIV, and WWH, both with TB and sPTB, had higher mRNA expression than WWoH with TB. Perturbations in and mRNA expression may be associated with inflammation related to HIV infection and spontaneous preterm birth, suggesting that further studies of S1P signaling in pregnancy, especially among women with HIV, are warranted. - Source: PubMed
Publication date: 2026/05/14
Resop Rachel SMwape InnocentSebastião Yuri VRittenhouse Katelyn JSindano NtazanaMwape HumphreyKasaro Margaret PVwalika BellingtonPrice Joan TStringer Jeffrey S ADe Paris Kristina - Sphingolipids regulate essential cellular processes, with sphingosine-1-phosphate (S1P) emerging as a critical modulator of proliferation, migration, and differentiation. While intracellular S1P governs sphingolipid metabolism during renal epithelial differentiation, its role as a ligand for S1P receptors (S1PRs) remains poorly understood. Here, we investigated the roles of S1PR1, S1PR2, and S1PR3 during the differentiation of Madin-Darby canine kidney (MDCK) cells. We found that S1PR2 and S1PR3 are critical for apical membrane formation, while S1PR2 additionally regulates adherens junction (AJ) maturation and actin cytoskeleton reorganization, essential for a differentiated epithelial morphology. Functional assays, including pharmacological inhibition and genetic silencing, showed that inhibition of S1PR2 impaired AJ formation and disrupted epithelial differentiation. Notably, S1PR2 restoration re-established AJ formation and epithelial organization, which underscores its critical role in maintaining cell-cell adhesion. Interestingly, S1PR2 exhibited distinct localization patterns throughout the differentiation process, transitioning from predominantly intracellular structures in proliferating cells to a more discrete peripheral/plasma membrane distribution along cell-cell boundaries in differentiated cells. These findings provide new insights into the spatial regulation of S1P signaling during renal epithelial differentiation and highlighted the emerging role of S1PR signaling in epithelial cell organization. This work broadens our understanding of S1PR2 mechanisms and suggests differential roles across stages of epithelial differentiation, thus offering potential therapeutic strategies for conditions involving renal epithelial dysfunction. - Source: PubMed
Publication date: 2026/05/08
Romero Daniela JudithPescio Lucila GiseleLoiacono GermánPalavecino Agustín NicolásFernández Federico EmanuelAlvarez Maria BelénSantacreu Bruno JaimeGuaytima Edith Del ValleFavale Nicolás Octavio - Lymph node metastasis (LNM) is a pivotal determinant of poor prognosis in ovarian cancer (OC), yet how tumor-intrinsic programs remodel the microenvironment to enable spread remains unclear.Here, we identify the transcription factor mesenchymal homeobox 1 (MEOX1) as an upstream coordinator, whose overexpression associates with LNM, increased lymphatic density, and poor survival based on integrative analyses of public datasets and our 113-patient cohort. In an in vivo LNM model, MEOX1 overexpression enhances tumor burden, lymphatic vessel density, and LNM, whereas tumor-conditioned medium does not directly activate lymphatic endothelial cells (LECs), implicating stromal intermediates. Spatial transcriptomic and immunostaining analyses confirmed cancer-associated fibroblast (CAF)-LEC proximity and vascular endothelial growth factor-C (VEGF-C) localization within CAFs, supporting a CAF-dependent lymphangiogenic route. Mechanistically, MEOX1 binds the sphingosine kinase 1 (SPHK1) promoter to activate sphingosine-1-phosphate (S1P) synthesis, driving a dual autocrine-paracrine program: sphingosine-1-phosphate receptor 3 (S1PR3)-dependent signaling promotes tumor proliferation/migration, while S1P/S1PR1 reprograms fibroblasts into VEGF-C-secreting, alpha-smooth muscle actin (α-SMA)-positive CAFs that stimulate lymphangiogenesis and LNM; SPHK1 inhibition blunts these phenotypes, whereas S1P supplementation restores them. These findings provide novel insights into lymphatic metastasis and demonstrate that metastatic competence depends not only on intrinsic tumor aggressiveness but also on the acquired ability to construct a pro-dissemination niche. - Source: PubMed
Publication date: 2026/05/10
Li JiajiaZhi XiulingLin QianhanSun YatingSun YihuaAbudousalamu ZulimireXue MengyangZheng ChangLi XiaotianYao LiangqingChen Mo - The third-generation EGFR tyrosine kinase inhibitor (TKI) osimertinib (AZD9291) has significantly improved the survival in EGFR-mutant lung cancer patients. Our team developed limertinib (ASK120067), a novel third-generation EGFR inhibitor with remarkable antitumor effects, which has been launched in China. Despite initial therapeutic responses, EGFR TKIs-treated patients ultimately experience fatal metastatic recurrence and disease progression. However, the underlying mechanism of driving metastasis remains poorly understood. Here, we aim to investigate the pro-metastatic mechanism following treatment with third-generation EGFR TKIs. Transcriptomics analyses of EGFR TKI-resistant tumor models revealed an aberrant upregulation of S1PR3, which conferred enhanced metastatic potential to lung cancer. S1PR3 inhibition dramatically reduced metastasis in resistant cells, while its overexpression potentiated metastatic abilities in parental cells. Notably, S1PR3 was highly enriched in clinical samples with AZD9291 resistance and correlates with poor prognosis. Mechanistically, we found that S1PR3 upregulated RAC1-GTP expression to activate PAK1, thereby promoting epithelial-mesenchymal transition (EMT) and enhancing metastatic capacity of resistant cells. Further studies identified that the overexpression of fibroblast growth factor receptor 1 (FGFR1) increased S1PR3 expression through signal transducer and activator of transcription 4 (STAT4) to promote the emergence of metastatic-resistant cells. Importantly, targeting S1PR3 or FGFR1 blocks metastasis in EGFR TKI-resistant models. - Source: PubMed
Publication date: 2026/04/23
Lai MengzhenChen JiayingQin YeZhang HuiPan ZiluZhang TaoTong LinjiangTang HaotianBai GangLiu QiupeiLi YanFeng FangSong PeiranLiu YingqiangChen YiFang YanTang BencanGeng MeiyuYu KerChen HaoDing JianXie Hua - Pancreatic ductal adenocarcinoma (PDAC) frequently exhibits perineural invasion (PNI), a clinicopathologic feature strongly associated with local recurrence and poor survival, yet lacking effective targeted interventions. By integrating patient cohorts with single-cell and bulk transcriptomics, multiplex immunofluorescence, and functional assays, this study defines a stromal-tumor signaling axis facilitating neural invasion. Cancer-associated fibroblasts (CAFs), particularly a myofibroblastic CAF-enriched population, upregulate sphingosine kinase 1 (SPHK1) and increase secretion of sphingosine-1-phosphate (S1P), which activates sphingosine-1-phosphate receptor 3 (S1PR3)/JNK/JUN signaling to transcriptionally induce MAL-like protein (MALL) in cancer cells. MALL binds to syndecan-4 (SDC4) and promotes its recycling to the plasma membrane, thereby increasing surface SDC4 abundance. This MALL-SDC4 program promotes RhoA/phosphorylated myosin light chain 2 (p-MLC2)-dependent amoeboid motility and sensitizes cancer cells to Schwann cell-derived pleiotrophin, strengthening directed neural invasion. Disruption of the axis through SPHK1 knockdown in CAFs, genetic perturbation of MALL or SDC4 in cancer cells, or adeno-associated virus-mediated SPHK1 or SDC4 knockdown in KPC (Kras; Trp53; Pdx1-Cre) mice significantly reduces PNI and tumor burden. These findings uncover a metabolite-driven MALL-SDC4 program connecting stromal metabolism to neural invasion, and identify promising therapeutic targets for PDAC. - Source: PubMed
Publication date: 2026/04/22
Peng WangCao MengdieHuang HaiBai ShuyaLiu LuyaoLiang JingwenCui HaochenZhou QiaodanChen ShiruJiang JiameiLiu LuoxiaLuan ZhouChen WeiXiong SiWang RonghuaCheng BinZhao Yuchong