Ask about this productRelated genes to: Sox2 protein
- 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 protein
Related articles to: Sox2 protein
- Upper tract urothelial carcinoma (UTUC) is a rare subtype of urothelial malignancy associated with poor prognosis, particularly in advanced stages. Sex determining region-Y-related high mobility group box 2 (SOX2), a key transcription factor involved in the maintenance of cellular stemness, has been identified as a potential biomarker in multiple cancer types; however, its prognostic significance in UTUC remains unclear. The present study aimed to investigate the expression pattern of SOX2 in UTUC and examine its association with clinicopathological characteristics. Moreover, the present study aimed to evaluate the association of SOX2 with programmed cell death ligand 1 (PD-L1) and antibody-drug conjugate (ADC) targets, including Nectin-4 and trophoblast cell surface antigen 2, to explore potential therapeutic implications. A total of 87 patients with UTUC who underwent radical nephroureterectomy were retrospectively analyzed. SOX2 expression was assessed using immunohistochemistry with a 10% cut-off value. Notably, SOX2 expression was detected in 24% (21/87) of cases. No significant associations were observed between SOX2 expression and clinicopathological parameters, molecular subtypes, or the expression of PD-L1 and ADC targets, except for hydronephrosis grade. Patients with SOX2-positive tumors exhibited significantly worse overall survival (OS), cancer-specific survival (CSS) and recurrence-free survival (RFS; P=0.004, P=0.005 and P=0.011, respectively) during a median follow-up period of 39.3 months. The 5-year CSS rates were 69% in the SOX2-negative group and 43% in the SOX2-positive group. Multivariate analysis identified SOX2 expression as an independent prognostic factor for CSS (P=0.001). Among patients who did not receive perioperative chemotherapy, those with SOX2-positive tumors demonstrated significantly poorer OS, CSS and RFS, compared with SOX2-negative patients. These findings indicated that SOX2 expression represents an independent and robust prognostic biomarker in UTUC, identifying a biologically distinct high-risk subgroup with unfavorable clinical outcomes. The preserved expression of PD-L1 and ADC targets in this subgroup may suggest potential responsiveness to immune checkpoint inhibitors and ADC-based therapies, supporting the consideration of intensified perioperative or systemic treatment strategies in SOX2-positive patients. - Source: PubMed
Publication date: 2026/04/28
Yasukawa HitomiIkehata YoshinoriNishiyama NaotakaKitamura Hiroshi - Cancer stem cells (CSC) role in treatment resistance is well established. CSCs promote M2 macrophage polarization within the tumor microenvironment, creating a pro-tumorigenic feedback loop that sustains CSC homeostasis. Therefore, disrupting this cross-talk can be an effective therapeutic strategy. In the present study, we identified Morusin as a potent inhibitor that could impact both cancer stemness and CSCinduced macrophage polarization. - Source: PubMed
Publication date: 2026/05/06
Tripathi TanyaJoshi UditChaudhary ApoorvaJanjua DivyaKumar ShivamTanwar NehaMittal AasthaSenrung AnnaBharti Alok Chandra - Heme oxygenases, HO-1 (Hmox1) and HO-2 (Hmox2), regulate skeletal muscle homeostasis by degrading heme and generating carbon monoxide (CO), a bioactive signalling molecule. Although HO-1 is known to influence muscle fibre composition and mitochondrial function, the role of HO-2 in activity-dependent neuromuscular plasticity remains poorly understood. This study aimed to define the distinct contributions of each isoform and test whether CO could restore muscle function in HO-deficient states. - Source: PubMed
Alves de Souza Rodrigo WIn Kim HyoAlves Paula Ketilly Nascimentoda Paixão Ailma OliveiraRasmussen AshleeShankar SidharthHarbison JamesVoltarelli Vanessa AzevedoOtterbein Leo E - Glioblastoma (GBM) remains a therapeutic challenge due to its resistance to standard chemotherapy and high recurrence rate. This study investigates the combined effects of alantolactone (ALT) and temozolomide (TMZ) on GBM cells, focusing on stemness, lipid metabolism, and the underlying Hippo signaling pathway. Human GBM cell lines U87 and U251 were treated with ALT and TMZ, either alone or in combination. Cell viability was assessed using the CCK-8 assay, stemness was evaluated by sphere formation assay, and gene and protein expression were analyzed by qPCR and Western blotting. A xenograft mouse model was established to evaluate in vivo efficacy. Phospho-kinase arrays and rescue experiments using the Hippo pathway inhibitor XMU-MP-1 were performed to explore the underlying mechanisms. The results showed that both ALT and TMZ inhibited cell proliferation in a dose-dependent manner. The combination treatment synergistically reduced cell viability, sphere formation, and the expression of stemness markers (CD133, NANOG, SOX2) and lipid metabolism regulators (PLIN2, FASN, SREBP1). In vivo, combined therapy significantly suppressed tumor growth and improved histopathological features. Mechanistically, ALT and TMZ promoted YAP1 phosphorylation and downregulated TEAD2, AXL, and c-MYC. Inhibition of Hippo signaling with XMU-MP-1 reversed the anti-tumor effects of the combination treatment. In conclusion, ALT and TMZ synergistically inhibit GBM growth and stemness by activating the Hippo pathway and suppressing lipid metabolism. These findings provide a rationale for the combined use of ALT and TMZ as a potential therapeutic strategy against GBM. - Source: PubMed
Publication date: 2026/05/13
Ren TongLi YishiZhou ChuanguangJiao YongqingGuo TianlinLi ZhiHu ChunyanZhao JunfengWang Xun - Aberrant sialylation is a persistent glycosylation change in cancer that reshapes interactions within the tumour microenvironment through the display of sialylated glycans (sialoglycans) on malignant and stromal cells. Many sialoglycans engage sialic acid-binding immunoglobulin-like lectins (Siglecs), a family of receptors expressed predominantly by immune cells that frequently transmit inhibitory signals and function as glyco-immune checkpoints. Increasing evidence indicates that tumour hypersialylation suppresses myeloid and lymphoid anti-tumour activity, promotes immune evasion, and contributes to metastatic behaviour. However, both sialoglycan repertoires and Siglec expression patterns vary markedly across cancer types and disease states, suggesting strong dependence on tissue context and tumour composition. In the present review, we discuss how tissue-of-origin programmes and lineage state establish basal sialyltransferase expression and constrain the sialoglycan landscape available to tumours. We highlight emerging single-cell evidence that stromal populations, particularly cancer-associated fibroblasts, can acquire hypersialylation and actively generate immunosuppressive Siglec ligands. We also examine how transcriptional and oncogenic regulators, including SOX2, MYC, and androgen receptor signalling, reprogramme sialyltransferase expression to produce tumour-specific sialoglycan profiles. Finally, we consider how standard-of-care therapies alter both ligand availability and immune composition, thereby dynamically modifying the sialoglycan-Siglec axis during treatment and resistance. Understanding these context-dependent determinants will be critical for interpreting sialylation in cancer biology and for designing effective therapeutic strategies targeting sialoglycan-Siglec interactions. - Source: PubMed
Wills JamieDuxfield AdamSiaka Monthe ManuellaScott Emma