Nanog antibody
- Known as:
- Nanog (anti-)
- Catalog number:
- orb69526
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Nanog antibody
Related genes to: Nanog antibody
- Gene:
- NANOG NIH gene
- Name:
- Nanog homeobox
- Previous symbol:
- -
- Synonyms:
- FLJ12581, FLJ40451
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-10
- Date modifiied:
- 2014-11-19
Related products to: Nanog antibody
Related articles to: Nanog antibody
- This study aims to elucidate the role of suppressor of cytokine signaling 3 (SOCS3) in glioma stem cells (GSCs) via single-cell RNA sequencing (scRNA-seq), focusing on its regulation of STAT3-mediated self-renewal, apoptosis resistance, and tumor microenvironment (TME) remodeling. ScRNA-seq data from 19 high-grade glioma patients were analyzed using Seurat, Harmony, and SingleR for clustering, annotation, and SOCS3 stratification (SOCS3-High: = 4; SOCS3-Low: = 15). Differential gene analysis, pathway enrichment, and CellChat were employed for TME characterization. In vitro, SOCS3-overexpressing/silenced GSC11 models were tested via MTT, TUNEL, neurosphere assays, and STAT3 pathway modulation (IL-6). In vivo, intracranial xenografts in nude mice evaluated tumor growth and survival. SOCS3 was downregulated in GSCs and neurons. SOCS3-Low GSCs exhibited 777 differentially expressed genes enriched in T-cell receptor, p53, and JAK-STAT axis, suppressed T-cell/microglia infiltration, and promoted oligodendrocyte precursor cell/astrocyte survival. SOCS3 overexpression reduced GSC proliferation, induced apoptosis, inhibited neurosphere formation, and suppressed STAT3 phosphorylation and stemness markers (OCT4/SOX2/NANOG). IL-6 reactivated STAT3, reversing SOCS3-mediated tumor suppression. In vivo, SOCS3 overexpression attenuated tumor growth and prolonged survival, counteracted by IL-6. Low SOCS3 expression contributes to glioma progression by promoting STAT3 activation and an immunosuppressive TME. Targeting the SOCS3-STAT3 axis may offer therapeutic potential. - Source: PubMed
Publication date: 2026/08/01
Wang JingtaoHou GaoleiSong ZhaofeiGao KaiWang HongbinLi Tao - Glioblastoma cells strongly express the tryptophan-metabolizing enzyme indoleamine 2,3-dioxygenase 1 (IDO1), which is important in enabling immune evasion. Notably, glioma stem-like cells (GSCs) express higher levels of IDO1 than differentiated glioblastoma cells (DGCs); therefore, it was hypothesized that IDO1 inhibition in GSCs may induce differentiation. The present study used the glioblastoma cell line U-87MG, and newly established GSC lines 0125-GSC and 0222-GSC. A model GSC line, Rev-U-87MG, was created by culturing U-87MG in serum-free medium. Rev-U-87MG-IDO(-) was generated by continuous treatment with an IDO1 inhibitor. The DGC lines 0125-DGC and 0222-DGC were derived by culturing 0125-GSC and 0222-GSC in serum-containing medium. IDO1-inhibited GSC lines 0125-GSC-IDO(-) and 0222-GSC-IDO(-) were generated by continuous IDO1 inhibitor exposure. The expression levels of IDO1 and stem cell markers (Nestin, Nanog and Sox2) were measured by western blotting, and temozolomide sensitivity was evaluated by cell counting. Notably, U-87MG, 0125-DGC and 0222-DGC adhered without sphere formation. By contrast, Rev-U-87MG, 0125-GSC and 0222-GSC formed spheres, whereas IDO1-inhibited cells showed partial adhesion with reduced sphere formation. IDO1 and stem cell marker expression were reduced in all IDO1-inhibited cell lines. Rev-U-87MG exhibited decreased temozolomide sensitivity compared with U-87MG, whereas Rev-U-87MG-IDO(-) showed increased sensitivity. Similarly, 0125-DGC and 0222-DGC were more sensitive than their parent GSC lines, and 0125-GSC-IDO(-) and 0222-GSC-IDO(-) also exhibited enhanced drug sensitivity compared with their parent GSC lines at multiple concentrations. These findings suggest that IDO1 inhibition may induce the differentiation of GSCs and reduce their resistance to temozolomide. - Source: PubMed
Publication date: 2026/07/21
Nishide KaoruYamamuro ShunAida YumiOzawa YoshinariSano EmikoYoshino Atsuo - Nanog, a transcription factor, is involved in cancer initiation and progression. - Source: PubMed
Ma LiliLu LinLiu XiaohuiWang LeiLiu YanWang YaqiLiu YankunZhang JinghuaLi Yufeng - Small intestinal adenocarcinoma (SIAC) is a rare malignancy with a rising incidence and poor prognosis. Although exportin-7 (XPO7) is typically characterized as a tumor suppressor, recent evidence suggests context-dependent oncogenic functions, yet its role in SIAC remains unexplored. This study evaluated the clinicopathological significance of XPO7 expression and its association with status, autophagy, and cancer stemness in 191 surgically resected primary SIAC cases using immunohistochemistry and automated digital quantification. XPO7 was significantly upregulated in SIAC compared to normal mucosa ( < 0.001). High XPO7 expression, observed in 27.2% of cases, correlated with higher histological grade ( = 0.023) and was identified as an independent predictor of poor overall survival (hazard ratio = 1.703; = 0.008). Subgroup analysis revealed that high XPO7 levels were associated with significantly shorter median overall survival specifically in cases featuring lymphovascular invasion, nodal metastasis, and mutations. Furthermore, XPO7 expression demonstrated a significant positive correlation with autophagy markers (LC3B and p62) but not with stemness markers (Sox2, Oct4, and Nanog). In conclusion, XPO7 serves as a significant independent prognostic biomarker for SIAC, and its correlation with autophagy markers in aggressive subgroups highlights its potential as a promising therapeutic target. - Source: PubMed
Publication date: 2026/07/19
Kim Jeong WonYlaya KrisChung Eun JooJun Sun-YoungHong Seung-MoChung Joon-Yong - Extracellular vesicles (EVs) participate in tumor progression and immune regulation through the transfer of bioactive molecules. Although tumor-derived EVs are generally considered to promote metastasis, accumulating evidence suggests that their functions vary according to the biological characteristics of their cells of origin. This study investigated the mechanisms underlying the anti-metastatic effects of EVs derived from -overexpressing melanoma cells (F10-EVs). - Source: PubMed
Publication date: 2026/07/08
Nakano MisatoTamura AsukaYorikawa SoraMatsuki NahokoIto RunaMatsuoka HideakiSaito Mikako