MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Known as:
- MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Catalog number:
- arp32018_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MEOX1 Antibody - C-terminal region (ARP32018_P050)
Related genes to: MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Gene:
- MEOX1 NIH gene
- Name:
- mesenchyme homeobox 1
- Previous symbol:
- -
- Synonyms:
- MOX1
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-14
- Date modifiied:
- 2016-11-09
Related products to: MEOX1 Antibody - C-terminal region (ARP32018_P050)
Related articles to: MEOX1 Antibody - C-terminal region (ARP32018_P050)
- Osteoporosis is a highly heritable metabolic bone disorder characterized by low bone mass and increased fracture risk. However, the causal genes underlying disease susceptibility remain incompletely understood. In this study, we employed a summary-data-based Mendelian randomization (SMR) framework to identify genes with potential causal effects on osteoporosis by integrating genome-wide association study summary statistics from the FinnGen consortium with multilayer molecular quantitative trait loci (xQTL) data, including expression, splicing, methylation, and protein QTLs across multiple tissues (106 xQTL datasets in total). The heterogeneity in dependent instruments (HEIDI) test was applied to distinguish pleiotropic associations from linkage disequilibrium-driven effects. Functional characterization was further conducted using Gene Ontology and KEGG pathway enrichment analyses, protein-protein interaction network construction, drug-gene enrichment analysis, and molecular docking. Using this integrative approach, we identified 15 high-confidence genes - CEP112, CKB, GID4, MEOX1, MEPE, PPP6R3, RGS9, RSPO3, SERPINA1, SFRP4, SOST, SPP1, SREBF1, TOM1L2, and ZBTB48 - showing evidence of causal associations with osteoporosis after stringent multiple-testing correction and HEIDI filtering. These genes included established regulators of bone metabolism as well as novel candidates involved in metabolic regulation and signal transduction. Enrichment analyses highlighted pathways related to Wnt and bone morphogenetic protein signaling, extracellular matrix organization, and metabolic processes, while network analysis revealed substantial functional connectivity among the prioritized genes. In addition, drug-gene enrichment analysis prioritized β-carotene, apocarotenal, and bezafibrate as potential therapeutic candidates, with molecular docking supporting stable interactions with key protein targets. Overall, this study provides robust genetic evidence for causal molecular regulators of osteoporosis and highlights potential therapeutic targets, offering a clinically relevant resource for future functional validation and translational research. - Source: PubMed
Yu FeiWan XiwenQiu Jiaxuan - Salivary adenoid cystic carcinoma (SACC) is a malignant salivary gland neoplasm characterized by aggressive local invasion and a marked propensity for metastasis. However, the role of MEOX1 in SACC progression remains poorly defined. In this study, we examined the effects of MEOX1 overexpression on the malignant behavior of SACC cells in vitro and in vivo. Human SACC-83 and SACC-LM cells were transduced with lentiviral vectors encoding MEOX1 or an empty vector control, and cell proliferation, migration, invasion, and cell cycle distribution were assessed using CCK-8, wound healing, Transwell, and flow cytometric assays, respectively. RNA sequencing was performed to characterize transcriptional changes associated with MEOX1 overexpression. In vivo, tumor growth was evaluated in BALB/c nude mice bearing subcutaneous xenografts, and pulmonary metastatic colonization was assessed using a tail vein injection model. MEOX1 overexpression reduced the proliferation, migration, and invasion of SACC cells in vitro and increased the G2/M phase fraction. In xenograft models, MEOX1-overexpressing cells formed smaller tumors and showed lower Ki67 staining than control cells. In the experimental lung metastasis model, mice injected with MEOX1-overexpressing cells developed fewer pulmonary metastatic nodules. RNA-seq identified 588 differentially expressed genes associated with MEOX1 overexpression, with enrichment in pathways including cytokine-cytokine receptor interaction, Toll-like receptor signaling, and G protein-coupled receptor signaling. Together, these findings indicate that enforced MEOX1 expression is associated with reduced malignant phenotypes in SACC models and with transcriptomic alterations in pathways related to immune response, G protein-coupled receptor signaling, and DNA damage response. - Source: PubMed
Publication date: 2026/05/06
Sun HuaxiuLiu YupingCui YajuanZhou ZhengWu ZhanlanZhou Chuan-Xiang - Mesenchyme homeobox 1 (MEOX1) has been characterised as a central transcriptional regulator of fibroblast activation. Ligustilide (LIG) has significant antifibrotic, anti-inflammatory and antioxidative activities. We investigated if LIG can ameliorate hepatic fibrosis by targeting MEOX1 and exploring the underlying mechanism. - Source: PubMed
Publication date: 2026/05/12
Luan QinrongWang ZhechengWang YueXu JialiWang GuorongHu ZhehaoZhou JunjunTian XiaofengZhao YanYao Jihong - 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 - Idiopathic pulmonary fibrosis (IPF) is a devastating chronic lung disorder with limited treatment options. Macropinocytosis is one of the key cellular processes involved in nutrient consumption from the extracellular environment under stress conditions. Here, we studied the role of macropinocytosis in experimental pulmonary fibrosis models. We found that macropinocytosis is increased in human lung fibroblasts (HLFs) derived from IPF patients. The inhibition of macropinocytosis with 5-(n-ethyl-n-isopropyl)-amiloride (EIPA) inhibited profibrotic responses in IPF-derived and TGF-1-stimulated HLFs and reduced pulmonary fibrosis in bleomycin (Bleo)-injured mice. EIPA exerted its antifibrotic effects by regulating amino acid (AA) uptake, mammalian target of rapamycin complex 1 (mTORC1) activation and mesenchyme homeobox1 (MEOX1) expression in activated HLFs. Fittngly, genetic inhibition of macropinocytosis also ameliorated lung fibroblast activation and pulmonary fibrosis in mice. Using IPF-derived precision cut lung slices (PCLS), we observed robust repression of profibrotic gene expression programs in EIPA-treated PCLS across different fibroblast subpopulations. Finally, we found that imipramine (Imi), a tricyclic antidepressant approved by the Food and Drug Administration (FDA), effectively inhibited macropinocytosis and ameliorated profibrotic responses in lung fibroblasts, Bleo-injured mice and IPF-derived PCLS. Taken together, our results suggest macropinocytosis inhibition can be considered as a potential therapeutic strategy to treat pulmonary fibrosis. - Source: PubMed
Publication date: 2026/04/30
Rosas Ivan OMcDowell-Sanchez Aaron KSanchez SantiagoCala-Garcia Juan DWaich Cohen Alan RRuiz-Echartea ElisaOchsner Scott AKraushaar Daniel CCelada Lindsay JSun DandanPolverino FrancescaCoarfa CristianMcKenna Neil JTsoyi Konstantin