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
- During the practice of diagnostic pathology, we identified a case of invasive ductal carcinoma (IDC) of the breast with lung metastases exhibiting a ductal carcinoma in situ (DCIS)-like morphology. Immunohistochemistry confirmed the presence of CK5/6, P40 and P63-positive tumor cells at the periphery of the metastatic nests. Subsequent expansion of our sample revealed similar DCIS-like morphology in lymph node metastases of other IDC cases. This study aimed to preliminarily characterize the pathological features, significance, and mechanisms of this phenomenon. - Source: PubMed
Publication date: 2026/09/30
Lin XinFan MingmeiLiu JingquanLong TingGao LingfangWu HaibinZhong YanLin WenwenWang RuianLi ZuguoChen Meihua - Progressive disease (PD) remains the dominant barrier to cure in high-risk neuroblastoma (HR-NB), driven in part by profound post-transcriptional deregulation that fuels clonal evolution, stemness, immune evasion, and therapy resistance. In this study, we define the molecular architecture of PD-associated microRNA (miR) collapse and demonstrate that radiotherapy (RT) acts as a potent post-transcriptional reprogrammer capable of reversing this trajectory. - Source: PubMed
Narayanan SivasubramaniSubramanian PoorviMohanvelu SreenidhiAravindan SheejaPeriyasamy LoganayakiAravindan Natarajan - The malignant progression of nonsmall cell lung cancer (NSCLC) is closely related to cancer stemness. Histone deacetylase 4 (HDAC4) plays a regulatory role in lung cancer, but its effect on NSCLC stemness remains unclear. This study aimed to investigate the role and mechanism of HDAC4 in NSCLC stemness. - Source: PubMed
Chen ChangxianJiang XiaomingYao ZhenwuSun JiaxueZhang LijuXu MingyuBao WeiminLiu Weijun - Bisphenol A (BPA) is a widespread plasticizer widely used in the food industry worldwide. However, a consensus on the safe level of its daily intake does not currently exist, while there are numerous data pointing to a link between prenatal exposure to BPA and early neuropsychiatric disorders, such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). The global average human-equivalent dose of BPA is estimated at 30 ng/kg body weight/day. Thus, the research herein was conducted on newborn and juvenile rat offspring of both sexes delivered from rats treated with 30 ng/kg body weight/day orally from day 6 to 21 of pregnancy and for a further 21 days during lactation. Our data indicate that prenatal exposure to 30 ng/kg/day from gestation day 6 to delivery induced sexually dimorphic, region-specific alterations in the neonatal (PD1) rat brains, impacting inflammatory reactions, estrogen receptor signaling, and neural progenitor dynamics. Prenatally BPA-treated males exhibited a pro-inflammatory state characterized by an increased total number of ramified Iba1+ microglia cells in the hippocampus alongside upregulation of , , , , and . Conversely, prenatally BPA-treated females showed only an increased total number of hippocampal Iba1+ cells and displayed inflammatory resilience, lacking upregulation of these markers. Both sexes exhibited a pro-inflammatory state in the prefrontal cortex via upregulation of , , , and . While both sexes showed decreased in the prefrontal cortex, they deployed distinct compensatory responses: males upregulated the neuroprotector only in the hippocampus, whereas in females, it was upregulated in both the hippocampus and the prefrontal cortex. Estrogen receptor expression was also highly dimorphic. In the hippocampus, males displayed an imbalance via upregulation and downregulation, while females showed downregulation alone. In the prefrontal cortex, these transcriptional profiles were the opposite. Finally, neural progenitor markers were altered. In the prefrontal cortex, BPA drove the upregulation of and in males but in females; in the hippocampus, only was upregulated, and only in males. The PAX6 protein level in the hippocampus was significantly increased in males but decreased in females. In juvenile offspring (PD21), behavioral patterns characterized by hyper-exploration, increased environmental investigation, and heightened emotional reactivity during social exposure were more pronounced in female offspring. These baseline neonatal disparities followed by behavioral changes underscore the necessity of sex-specific approaches when evaluating early-life neurodevelopment and subsequent adult behavioral and biological vulnerabilities. - Source: PubMed
Publication date: 2026/09/14
Gerasimov Andrey DSentyabreva Alexandra VGantsova Elena AMelnikova Ekaterina AKosyreva Anna M - Breast cancer stem cells (BCSCs) drive tumor progression, metastasis, and therapeutic resistance. Sirtuin 1 (SIRT1) has been implicated in stem cell regulation, but its context-dependent role in BCSC maintenance and the underlying molecular mechanisms remain poorly defined. SIRT1 expression was evaluated in human breast cancer specimens. Pharmacologic and genetic SIRT1 inhibition was assessed in breast cancer cell lines and orthotopic xenograft models to determine effects on stemness, epithelial-mesenchymal transition (EMT), metastasis, and chemoresistance, with emphasis on Wnt/β catenin signaling. SIRT1 was overexpressed in breast cancer and correlated with higher tumor grades. SIRT1 inhibition reduced BCSC markers (CD44, ALDH1), stemness genes (NANOG, SOX-2), mammosphere formation, EMT, and invasion. In vivo, SIRT1 inhibition suppressed tumor growth, blocked lymphatic metastasis, and delayed cisplatin resistance. Mechanistically, these effects were mediated by downregulation of Disheveled 3 (DVL3) and attenuation of Wnt/β catenin signaling. SIRT1 is associated with the maintenance of BCSC-related properties, EMT, and activation of the Wnt/β-catenin pathway in breast cancer. Targeting SIRT1 may represent a potential therapeutic strategy to suppress tumor progression and improve treatment response. - Source: PubMed
Publication date: 2026/09/15
Ding JianminGuan BaoxiangFan XuejunZhang NingyanSevick EvaZhang Songlin