SOX9
- Known as:
- SOX9
- Catalog number:
- ARP37986_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9
Related genes to: SOX9
- Gene:
- SOX9 NIH gene
- Name:
- SRY-box 9
- Previous symbol:
- CMD1, CMPD1
- Synonyms:
- SRA1
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-25
- Date modifiied:
- 2018-06-25
Related products to: SOX9
Related articles to: SOX9
- Tumour-associated macrophages (TAMs) are known to promote tumour progression in many kinds of malignant tumour, including hepatoblastoma (HB). Based on previous studies, we suggested that TAM-mediated sex-determining region Y-box 9 (SOX9) signal might enhance HB progression. The present study investigated the significance of the SOX9 signal in HB and examined the mechanisms underlying cell-cell interactions between tumour cells and TAMs. Co-culture with human monocyte-derived macrophages increased SOX9 expression in HB cell lines. Immunohistochemical analysis of HB samples revealed a positive correlation between SOX9 expression and TAM infiltration, and SOX9 expression was predominantly observed in the embryonal subtype. Increased SOX9 expression was associated with shorter 5-year recurrence-free and overall survival. Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signalling was found to be involved in macrophage-induced SOX9 upregulation. The Wnt/β-catenin pathway was also activated by co-culture with macrophages and appeared to be upregulated by SOX9 expression. In summary, SOX9 was identified as a poor prognostic factor in HB, with expression enhanced by macrophage-derived factors. The YAP/TAZ and Wnt/β-catenin pathways are critical for cell-cell communication and are linked to SOX9 overexpression. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/08/27
Hirao HirokiAdawy AhmadFujiwara YukioYoshii DaikiPan ChengLi LianboYano HiromuKondo YoshihikoHonda MasakiHan JiaLiu YaoYamada SohsukeHiyama EisoChunthaboon PaweenaponSakamoto YasuhisaMoroishi ToshiroYamamoto MasahiroHibi TaizoKomohara Yoshihiro - Hidradenitis suppurativa (HS) is increasingly recognized as a disorder of intrinsic dysregulation at the intersection of genetic susceptibility, host-microbial interactions, and hormonal signaling, with select environmental exposures acting as important secondary modifiers. This narrative review synthesizes mechanistic, clinical, and epidemiologic evidence on intrinsic and extrinsic contributors to HS pathogenesis. Genetic susceptibility for HS involves pathways regulating keratinocyte differentiation, epidermal stem cell function, and follicular architecture, including Notch signaling and transcriptional regulators such as SOX9 and KLF5. Microbiome alterations in both lesional and non-lesional skin suggest that early dysbiosis may contribute to follicular occlusion, epithelial disruption, and immune activation. Hormonal signaling, particularly androgen signaling, promotes follicular dysfunction and inflammation during periods of hormonal fluctuation, frequently aligning with the time of disease onset and flares. Environmental exposures vary considerably in the strength of supporting evidence: tobacco use and elevated body mass index have the most robust epidemiologic and mechanistic data, heat and humidity are increasingly recognized as disease activity modifiers, and evidence for air pollution and microplastics is growing. Collectively, these findings support a model in which HS arises from intrinsic follicular dysregulation shaped by genetic, microbial, and hormonal factors, with environmental exposures influencing but unlikely to independently initiate disease. - Source: PubMed
Publication date: 2026/08/13
Moslehi DorsaJohnson LannikaCharrow Alexandra PPastar Irena - Neuropathic pain (NP) is a debilitating chronic condition whose molecular mechanisms remain incompletely understood, limiting the development of effective disease-modifying therapies. Lactylation, a lactate-derived post-translational modification of histone and non-histone lysine residues, has recently emerged as a critical epigenetic mechanism that directly couples glycolytic activity to transcriptional reprogramming. Following peripheral nerve injury, four pain-relevant cell populations undergo cell-type-specific glycolytic reprogramming through distinct upstream cascades: the AREG-EGFR-PKM2 axis in dorsal root ganglion sensory neurons, RUNX1-CMPK2 in spinal microglia, Sox9-HK1 in spinal astrocytes, and LDHA in peripheral Th17 cells. The resulting intracellular lactate accumulation drives lactylation through three mechanistic modes: transcriptional activation of pro-nociceptive genes, silencing of analgesic mediators, and direct inactivation of pain-suppressive signaling proteins. A self-reinforcing feedback loop between glycolysis and lactylation further perpetuates the chronic pain state. This review synthesizes current mechanistic evidence, evaluates emerging pharmacological strategies targeting this metabolic epigenetic axis, and discusses outstanding translational challenges including reader protein identification, sex-based variability, and human tissue validation. - Source: PubMed
Publication date: 2026/08/26
Qin ZhengshanZeng YuanOu Cehua - Perfluorooctanesulfonic acid (PFOS), a persistent per- and polyfluoroalkyl substance, has been associated with male reproductive toxicity, but the underlying molecular mechanisms remain incompletely defined. Here, we show that chronic exposure to environmentally relevant doses of PFOS caused dose-dependent testicular injury and spermatogenic dysfunction in mice, as indicated by reduced testis weight, disrupted seminiferous tubule architecture, and impaired sperm quality. Transcriptomic profiling revealed marked enrichment of pathways related to oxidative stress, mitochondrial dysfunction, and reproductive regulation. Mechanistically, PFOS increased mitochondrial reactive oxygen species (ROS) production in GC-2 spermatocyte cells, leading to mitochondrial membrane potential collapse, lipid peroxidation, and depletion of antioxidant defenses. Pharmacological scavenging of mitochondrial ROS with Mito-TEMPO attenuated PFOS-induced mitochondrial injury in vitro and improved testicular damage and sperm quality in vivo. We further found that PFOS suppressed the RNA demethylase FTO and promoted its ROS-dependent redistribution from the nucleus to mitochondria, resulting in global mA hypermethylation. Integrated mA epitranscriptomic analysis showed that PFOS remodeled mA modification patterns on key transcripts involved in spermatogenesis, steroidogenesis, and redox homeostasis, including CYP11A1, SOX9, STRA8, and GPX4. FTO bound these transcripts, and restoration of FTO expression reversed PFOS-induced mA hypermethylation and rescued reproductive gene expression. Together, these findings identify a mitochondrial ROS-FTO-mA regulatory axis that links PFOS-induced mitochondrial oxidative stress to epitranscriptomic disruption and male reproductive dysfunction. Our study defines FTO-dependent RNA demethylation as a critical molecular mechanism and potential intervention target in PFOS-induced reproductive injury. - Source: PubMed
Publication date: 2026/08/26
Pang YipengYang ShiqingWang YuenanAmona Fructueux ModesteZhou RongLiu ZiluTian ChuanbeiChen Xi - Chemotherapy-induced testicular damage is a major cause of male infertility, primarily due to oxidative stress, apoptosis, and disruption of the spermatogonial niche. Spermatogonial stem cells (SSCs) as well as Sertoli cells are central regulators of spermatogenesis, and preserving their function is essential for maintaining male fertility. This study investigated the protective and regenerative potential of helium plasma-activated conditioned medium (PACM) against bleomycin-induced cytotoxicity in a neonatal rat SSCs-Sertoli cell co-culture model. Testicular cells were isolated and characterized using alkaline phosphatase assay and qRT-PCR for evaluating CD49f and Sox9 expression. Cells were treated with conditioned medium (CM), plasma-activated medium (PAM), and plasma-activated conditioned medium (PACM), either alone or in combination with bleomycin (Ble). Among all treatments, PACM exerted the strongest protective effects, significantly through enhancing cell viability and colony formation as well as reducing intracellular reactive oxygen species (ROS) and apoptosis. Based on findings, Ble markedly disrupted redox balance, apoptosis increment verified through Annexin-FITC externalization, suppressed Nrf2, c-KIT and CAT expression, attenuated catalase enzyme activity; however, co-treatment with PACM most effectively overwhelmed Ble insult, indicating activation of antioxidant defenses and spermatogenic signaling pathways. The superior efficacy of PACM appears to result from the synergistic interaction between plasma-generated reactive oxygen and nitrogen species (RONS) and the bioactive components of conditioned medium, including growth factors, cytokines, and exosomes. Collectively, these findings indicated that PACM restores the spermatogonial microenvironment, reinforces endogenous regenerative capacity, and offers a promising cell-free strategy to mitigate bleomycin-induced reproductive toxicity in vitro. It proposes that future studies are critical to identify the specific PACM components, the principal mediators and signaling pathways responsible for PACM effects. A graphical overview of the experimental workflow and outcomes is presented in Fig. 1. - Source: PubMed
Publication date: 2026/08/20
Keshvari LeilaAmini ElahehHajisharifi KamalAzarnia MahnazRobert Eric