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
- 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 - Cisplatin (CDDP) resistance constitutes the principal clinical challenge in the treatment of advanced non-small cell lung cancers (NSCLC). Disturbances in copper metabolism are closely linked with tumor drug resistance. SOX2, a pivotal stemness transcription factor (TF), holds an important role in chemotherapy resistance. However, whether it influences CDDP resistance by modulating cuproptosis remains unknown. SOX2 level was tested by qPCR and WB, and ATP7B level was evaluated by WB and flow cytometry. The oligomerization levels of FDX1, LIAS, and DLAT, together with Cu levels, were determined by WB, confocal microscopy, and a Cu colorimetric assay kit. The proliferation and apoptosis of NSCLC drug-resistant cells were assessed with CCK-8 and flow cytometry. SOX2 was significantly up-regulated in CDDP-resistant NSCLC cells, accompanied by decreased cuproptosis sensitivity. Silencing SOX2 in CDDP-resistant cells increased cuproptosis sensitivity and apoptosis rate and reduced cell viability. These effects of SOX2 silencing on CDDP resistance in NSCLC cells were reversed by the cuproptosis inhibitor TTM. SOX2 up-regulated ATP7B by activating the Wnt/β-catenin signaling pathway. Silencing ATP7B or treatment with the Wnt pathway inhibitor LF3 attenuated SOX2 overexpression-induced promoting effect on CDDP resistance and suppressive effect on cuproptosis in NSCLC. In summary, this study reveals a novel mechanism wherein SOX2 activates the Wnt/β-catenin signaling pathway to upregulate ATP7B expression, thereby suppressing cuproptosis and ultimately driving cisplatin resistance in NSCLC. These findings provide potential therapeutic targets for reversing chemoresistance in NSCLC. - Source: PubMed
Publication date: 2026/09/18
Chen KunHe Fu-MeiHuang Ying-HuiFang TingZheng Yi-PingCai Jian-Feng - Prostate cancer is aggressive in dogs and characterized by limited therapeutic responsiveness and a poor prognosis. While cancer stem cells (CSCs) are increasingly recognized as key drivers of tumour progression, therapeutic resistance and metastasis in human prostate cancer, their role in canine prostate cancer remains poorly defined. This study aimed to characterize the expression of stem cell-associated markers in canine prostatic adenocarcinoma by assessing a broad panel of CSC-associated markers in primary prostate tissues. Immunohistochemistry evaluated the expression and subcellular localization of seven CSC-associated markers (CD44, CD133, Nanog, Nestin, Oct3/4, Sox2 and Trop2) in non-neoplastic canine prostate samples and prostatic adenocarcinoma cases. Marker expression was semiquantitatively assessed and differences between groups analysed using non-parametric statistical tests. Neoplastic prostatic tissue demonstrated significantly increased immunolabelling of CD44, CD133, Nanog (nuclear and cytoplasmic), Nestin (nuclear and cytoplasmic), Oct3/4 (cytoplasmic), Sox2 (cytoplasmic) and Trop2 compared with non-neoplastic prostate tissue (P <0.05). In contrast, nuclear Oct3/4 and nuclear Sox2 immunolabelling did not differ significantly between groups. Distinct patterns of nuclear and cytoplasmic localization were observed for several markers, suggesting context-dependent regulation and potential functional heterogeneity within CSC-like populations. These findings demonstrate that canine prostatic adenocarcinomas have multiple stem cell-associated markers, consistent with the presence of a stemness-associated phenotype within these tumours. - Source: PubMed
Publication date: 2026/09/17
Story Michelle MFonseca-Alves Carlos ELaufer-Amorim ReneePalmieri Chiara