Sox2
- Known as:
- Sox2
- Catalog number:
- 000691A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Sox2
Related genes to: Sox2
- Gene:
- SOX2 NIH gene
- Name:
- SRY-box 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-30
- Date modifiied:
- 2019-04-23
Related products to: Sox2
Related articles to: Sox2
- Epithelial-mesenchymal transition (EMT) of medial edge epithelial cells is a critical mechanism underlying embryonic palatal fusion, driven by transforming growth factor beta 3 (TGF-β3). However, its regulatory interplay with pluripotency factors (SOX2/OCT4) and reliance on downstream cascades remain poorly understood. This study investigates these networks to elucidate the mechanisms of cellular reprogramming during palatogenesis. Embryonic day 15 C57BL6/J mouse palatal epithelial cells were isolated to eliminate mesenchymal interference. Cells were subjected to recombinant TGF-β3 (1, 3, 10 ng/mL) or targeted siRNA knockdowns of Tgfb3, Sox2, Oct4, and Smad2/3, and evaluated via RNA sequencing, qRT-PCR, immunofluorescence, TEER, and flow cytometry. Treatment with 1-3 ng/mL TGF-β3 successfully induced EMT in vitro, characterized by decreased E-cadherin, increased fibronectin, diminished membrane resistance, and a fibroblast-like morphological shift. This transition was predominantly associated with non-canonical pathways; phosphorylated Smad2/3 levels remained unchanged while Smad-independent mediators (p38 MAPK and Mmp13) were upregulated (p<0.05). Furthermore, TGF-β3 downregulated the pluripotency markers Sox2 and Oct4 (p<0.05). Combined Sox2/Oct4 knockdown with TGF-β3 yielded the most pronounced EMT characteristic. While Tgfb3 knockdown heavily attenuated EMT, partial mesenchymal transition persisted, indicating redundant compensatory networks. In conclusion, optimal TGF-β3 concentrations (1-3 ng/mL) shift EMT toward Smad-independent pathways during palatogenesis. This reprogramming requires TGF-β3 to suppress SOX2 and OCT4, underscoring their roles as negative regulators of EMT during palatal fusion. - Source: PubMed
Publication date: 2026/09/22
Mahatumarat NatchaSahmeddini SarinaAlvarez-Rivas CarlaAlves TomazCortez Leticia RojasMohammadi SabaVargas DorathyMotro MelihWill Leslie ATrackman Philip CKantarci Alpdogan - Glioblastoma (GBM) is the most aggressive primary brain tumor in adult patients and is characterized by significant cellular heterogeneity and complex interactions between tumor cells and the tumor microenvironment. Extracellular vesicles (EVs) and the microRNAs (miRNAs) they carry are important mediators of intercellular signaling and, at the same time, a potential source of biomarkers useful in the diagnosis of gliomas. Experimental models capable of preserving the biological properties of the original tumor are essential for studying these processes. In this study, we prepared glioblastoma organoids (GBOs) derived from patient tumor tissue and analyzed extracellular miRNAs present in EVs isolated from conditioned media. Concurrently, we analyzed miRNAs contained in EVs isolated from cerebrospinal fluid (CSF) of patients with gliomas of varying degrees of malignancy. A total of 12 GBOs cultures were successfully established, long-term cultured, and cryopreserved. Immunohistochemical analysis confirmed the presence of markers typical of glioblastoma cells (Nestin, GFAP, Sox2). In early-stage organoids, cell populations representing the tumor microenvironment were also detected, including endothelial cells (CD31) and microglia (CD163). In some cases, reactive astrocytes and neurons were also present. Highly abundant miRNAs were identified in EVs isolated from conditioned media of GBO and primary GBM cultures, including hsa-miR-21-5p, members of the let-7 family, hsa-miR-16-5p, hsa-miR-125b-5p, and others. These miRNAs were simultaneously detected in EVs isolated from the CSF of patients with GBM and high-grade gliomas. In contrast, miR-204-5p, which was predominantly present in CSF samples, was minimally represented in EVs from tumor cultures, suggesting a possible origin of this miRNA in non-tumor brain tissue. The presented data support the use of GBOs derived from patient tumor tissue as a suitable model for studying intercellular communication and extracellular signaling in GBM and simultaneously demonstrate the potential of EV-associated miRNAs as biomarkers of the tumor microenvironment. - Source: PubMed
Součková KSiegl FHýžďalová MPěnčíková KVaňková THendrych MFadrus PŠána J - Despite the contribution of cancer stem-like cells (CSLCs) to acquired paclitaxel resistance in non-small cell lung cancer (NSCLC), the biomarkers and regulatory mechanisms sustaining their stemness under chemotherapy pressure remain poorly understood. This study aimed to identify the stemness-maintaining programs underlying CSLC-associated paclitaxel resistance. Paclitaxel-resistant NSCLC cell models were established. RNA-seq data from resistant spheres and adherent resistant cells were integrated with Gene Ontology/Kyoto Encyclopedia of Genes and Genomes/gene set enrichment analysis and patient transcriptomic datasets to identify CSLC maintenance-associated candidate biomarkers. Inhibitors, sphere-forming assays, CD104CD166CD49f flow cytometry, reverse transcription quantitative polymerase chain reaction, western blotting, and ST6GAL1 knockdown or overexpression were used for functional and mechanistic validation. Sambucus nigra agglutinin lectin blotting was performed to assess epidermal growth factor receptor (EGFR) α2,6-sialylation. Clinical relevance was assessed using ST6GAL1 immunohistochemistry on 46 clinical lung tumor tissues. Paclitaxel-resistant NSCLC cells exhibited enhanced sphere formation and CD104CD166CD49f expansion. N-glycosylation was activated in resistant spheres. A seven-gene N-glycosylation signature was identified as a CSLC-associated candidate biomarker in acquired paclitaxel resistance. Inhibiting N-glycosylation suppressed the EGFR-mTOR-SOX2/BMI1 axis, decreased CSLCs, and restored paclitaxel sensitivity. ST6GAL1 regulated EGFR α2,6-sialylation. ST6GAL1 depletion also decreased EGFR abundance, suppressed mTOR-SOX2/BMI1 signaling, and sensitized paclitaxel-resistant spheres to paclitaxel rather than adherent cells. ST6GAL1 expression, which was higher in tumors from patients who underwent chemotherapy, showed a trend toward poorer survival among chemotherapy-treated patients. The seven-gene signature was associated with shorter disease-free survival but not overall survival in lung cancer patients. ST6GAL1-mediated α2,6-sialylation of EGFR contributes to the maintenance of CSLC-associated paclitaxel resistance through mTOR-SOX2/BMI1 signaling. These findings identify ST6GAL1-dependent EGFR sialylation as a potential therapeutic target in CSLC-associated chemoresistance. - Source: PubMed
Publication date: 2026/08/31
Yang YuxiLiang BinghuiHong WeijieLee Sau HarTang DongfangXie ShuxianQin ChangtaiShen LiuSun ZhumeiYan XiaofengLi HuaWang XiaolingHu XudongYe TingjieZhang WeiXu Wei - Zinc finger PBX1-interacting protein (Zfp462/Zfpip), a vertebrate-specific C2H2-type transcription factor, plays an essential role in early embryogenesis and the maintenance of embryonic stem cell (ESC) pluripotency. While previous studies have largely focused on its repressive functions, its potential role in transcriptional activation has remained unclear. In this study, we demonstrate that Zfp462 knockout (KO) impairs ESC self-renewal and disrupts the expression of pluripotency-associated and developmental genes. Luciferase reporter assays showed that Zfp462 overexpression increased (also known as ) promoter activity, whereas Zfp462 KO reduced its activity, supporting a role for Zfp462 in transcriptional activation. Integrative multiomics analyses reveal that Zfp462 is functionally integrated into the ESC core pluripotency module and cooperates with Oct4, Sox2, and Nanog to activate pluripotency-associated genes. Together, these findings reveal a critical role for Zfp462 in ESC pluripotency and establish it as a novel regulator within the pluripotency gene regulatory network. - Source: PubMed
Publication date: 2026/09/18
Yu MengYang YiChen ChunlinWang JiaqiYang WubinYang RanXu YixiaoWang FengshengZhang ChenZhang YangkaiDong YutongWang JiangjunXue RuoyiTian YanpingCui XiaopingRuan YanLi HongliZhang JunleiJian Rui - Sulfatide (3-O-sulfogalactosylceramide) is a major glycolipid component of myelin synthesized by oligodendrocytes in the central nervous system (CNS) and Schwann cells (SCs) in the peripheral nervous system (PNS). Although sulfatide diversity has been characterized in CNS myelin, its species-level composition, spatial organization, and developmental dynamics in the PNS remain poorly defined. Here, we used imaging mass spectrometry (IMS) to characterize sulfatide molecular species in murine dorsal root ganglia (DRGs) during development. Thirteen sulfatide species were identified in adult DRGs and classified as long-chain (LC) or very-long-chain (VLC), with hydroxylated or non-hydroxylated forms. VLC non-hydroxylated sulfatides were preferentially enriched in compact myelin-rich regions, whereas LC and hydroxylated species exhibited broader distributions extending into neuronal soma-associated regions. Multivariate analyses further demonstrated that regional sulfatide molecular species profiles were associated with fatty acyl chain length and hydroxylation status. Developmentally, structurally diverse sulfatide classes, including LC non-hydroxylated, VLC non-hydroxylated, and VLC hydroxylated species, were detectable by embryonic day 14.5, and all species were present by postnatal day 2, indicating that sulfatide diversification is established before mature myelin formation. Sulfatide species exhibited ventral enrichment within developing DRGs, a pattern partially conserved in chick embryos. Analysis of Cst-null mice confirmed previously reported abnormalities in myelinating SC-axon units and further revealed defective Remak bundle organization characterized by incomplete axonal ensheathment, together with altered dynamics of Sox10+/Sox2+ SCs. These findings reveal a previously unrecognized spatiotemporal heterogeneity of sulfatide species in the developing PNS and support roles for sulfatide diversity in SC maturation and peripheral nerve organization. - Source: PubMed
Gamo KeizoKoike TaroOe SoichiIwashita HikaruOkamura KohjiYamanaka HiroshiNakashima KeikoTanaka SusumuHayashi ShinichiSeki-Omura RyoheiSato YukiNakano YousukeKataoka YoskyOno KatsuhikoTsuda MasayukiHonke KoichiKitada MasaakiHirahara Yukie