Ask about this productRelated genes to: SOX9 antibody
- 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 antibody
Related articles to: SOX9 antibody
- Primary liver cancers, including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), arise from the neoplastic transformation of hepatocytes and cholangiocytes, respectively. Loss or downregulation of PTEN, a tumor suppressor negatively regulating the PI3K/AKT pathway, is frequently observed in CCA and HCC. Notably, PTEN mutations are observed at nearly twice the frequency in combined CCA-HCC tumors than either HCC or CCA alone. Using lineage-specific liver-targeted PTEN-deficient mouse models, we demonstrate that PTEN loss drives cellular dedifferentiation and tumorigenesis, a process that is critically dependent on AKT2. Mechanistically, PTEN deficiency induces activation of NOTCH and upregulation of transcriptional factor SOX9, which plays a central role in tumor cell transformation. In parallel, PTEN loss increases SMAD4 expression and sensitizes the tumor cells to TGFβ signaling, with TGFβ treatment repressing SOX9 expression in tumor cells lacking PTEN. Together, our study defined a critical role for PTEN-AKT2 signaling in maintaining liver epithelial lineage fidelity and revealed how its disruption promotes the conversion of mature hepatocytes or cholangiocytes into liver cancer stem-like cells (LCSCs). Furthermore, we identify a PTEN-dependent crosstalk between NOTCH and TGFβ pathways that governs liver tumor development. Together, this work provides mechanistic insight into lineage plasticity in liver cancer with implications for pathway-directed therapy. - Source: PubMed
Publication date: 2026/08/20
Tang QiSlarve IelyzavetaChen JingyuZeng NiGu YiweiHe LinaHu ShunanAlhousari DialaXu ZifeiHua BrittneyZhang GuoNguyen PhillipAlba MarioBharadwaj AjayLee JihyeonKreimer SimionXu JianJi BaoanLu Shelly CVan Eyk JenniferChopra ShefaliKanel GaryYuan LiyunStiles Bangyan L - Prednisone is commonly used to control autoimmune and inflammatory diseases during pregnancy, but its potential effects on fetal skeletal development remain incompletely characterized. This study investigated the dose- and exposure-period-related effects of prenatal prednisone exposure (PPE) on fetal long-bone development in mice and explored the cellular mechanism involving chondrocyte-to-osteoblast transdifferentiation. Pregnant mice received prednisone at 0.25 or 1.0mg/kg/day throughout gestation or 1.0mg/kg/day during defined gestational periods. Fetal femurs were collected on gestational day 18 (GD18) for histomorphometric, histochemical, and immunofluorescence analyses. PPE shortened fetal femurs, reduced the primary ossification center (POC), narrowed the proliferative zone (PZ), and expanded the hypertrophic zone (HZ), with generally greater changes after higher-dose or longer-duration exposure. Quantitative cellular analysis demonstrated fewer proliferative chondrocytes, accumulation of hypertrophic chondrocytes, and reduced osteoblast numbers within the POC. Consistently, PPE decreased SRY-box transcription factor 9 (SOX9) and runt-related transcription factor 2 (RUNX2) protein expression while increasing type X collagen (COL10) expression. The accumulation of hypertrophic chondrocytes, together with insufficient osteoblast formation, indicates that PPE impairs the cellular transition from hypertrophic chondrocytes to osteoblasts. Collectively, impaired chondrocyte-to-osteoblast transdifferentiation represents a cellular mechanism contributing to PPE-induced fetal long-bone dysplasia. - Source: PubMed
Publication date: 2026/08/20
Zhu JiayongXiao HaoWang HuiChen Liaobin - The quality of cashmere fiber is fundamentally determined by the embryonic morphogenesis of hair follicles, a process highly dependent on the normal function of hair follicle stem cells (HFSCs). MicroRNAs (miRNAs) are key post-transcriptional regulators, but their specific roles in cashmere goat hair follicle development remain unclear. In this study, we identified the differentially expressed miRNA, miR-376c-3p, by analyzing transcriptomic data from embryonic skin (E65, E90, E120) of cashmere goats. Functional assays, including CCK8, crystal violet staining, clonogenic assay, and analysis of proliferation/apoptosis-related proteins (PCNA, CDK4, MKI67, BCL2, CAS3 and CAS9), demonstrated that miR-376c-3p significantly inhibited HFSCs proliferation, induced apoptosis, and blocked the differentiation process, as evidenced by the downregulation of differentiation-associated keratins (KRT4, KRT10, KRT14) and the upregulation of stemness maintenance factors (OCT4, NANOG, SOX9 and KRT15). Mechanistic investigations revealed that miR-376c-3p directly bound to the 3'UTR of STRBP mRNA and inhibited its expression, which was validated by a dual-luciferase reporter assay. Conversely, overexpression of STRBP promoted HFSCs proliferation and differentiation. Further analysis found that STRBP functioned by activating the Wnt/β-catenin and BMP signaling pathways, whereas miR-376c-3p inhibited these same pathways. In summary, this study elucidates a novel regulatory axis: miR-376c-3p influencing the Wnt/β-catenin and BMP signaling cascades in HFSCs by targeting STRBP mRNA, thereby regulating cell fate. This research provides important insights into the molecular mechanisms of miRNA-mediated hair follicle morphogenesis and stem cell biology in cashmere goats. - Source: PubMed
Guo YiWang NiuHou XiaojieSun LongkangHe HulinWang Xin - Knee osteoarthritis (KOA) is characterized by progressive cartilage degeneration and inflammation. This study investigated the therapeutic effects of acupotomy in a rabbit model of KOA and its association with the circular RNA phosphodiesterase 4B (circPDE4B)/resistance to inhibitors of cholinesterase 8A (RIC8A)/p38 mitogen-activated protein kinase (MAPK) signaling axis. Fifty New Zealand White rabbits were randomly assigned to five groups (n = 10 per group): control, KOA model, celecoxib, acupotomy, and sham acupotomy. KOA was induced using the modified Videman method. Beginning 6 weeks after modeling, acupotomy was administered once weekly for 4 weeks, whereas celecoxib was administered daily by gavage at 24 mg/kg for 4 weeks. Knee swelling and cartilage histopathology were evaluated. Levels of interleukin-1β (IL-1β) , tumor necrosis factor-α (TNF-α) , and interleukin-6 (IL-6) in cartilage tissue homogenates were measured by enzyme-linked immunosorbent assay. Gene and protein expression associated with cartilage metabolism and the circPDE4B/RIC8A/p38 MAPK axis were assessed by quantitative reverse transcription polymerase chain reaction and Western blotting. Compared with the KOA model group, acupotomy reduced knee swelling, improved histopathological scores, decreased inflammatory cytokine levels, downregulated matrix metalloproteinase-3 (MMP-3) , matrix metalloproteinase-13 (MMP-13), RIC8A, and phosphorylated p38 MAPK, and upregulated SRY-box transcription factor 9 (SOX9), aggrecan, and relative circPDE4B. Its effects were comparable to those of celecoxib, whereas sham acupotomy produced no significant improvement. These findings indicate that acupotomy alleviates inflammation and cartilage degeneration in rabbit KOA and is associated with modulation of the circPDE4B/RIC8A/p38 MAPK axis. - Source: PubMed
Publication date: 2026/08/18
Luan Guo-RuiShang XiangZhao Han-QingMeng De-HongMa Rui-RuiHu ChenYang Yong-HuiLiu Cun Bin - Injectable hydrogels offer a minimally invasive approach for cartilage repair, enabling precise defect filling and in situ scaffold formation; however, balancing mechanical strength with stem cell viability and chondrogenic differentiation remains challenging. Here, alginate dialdehyde-gelatin (ADAG) hydrogels are reinforced with cellulose nanofibrils (CNFs) to enhance mechanical performance while retaining injectability, rapid self-healing, and chondroinductive properties. FTIR spectroscopy confirms efficient Schiff base cross-linking between ADA and gelatin, with CNF incorporation preserving chemical integrity. SEM imaging revealed a porous, interconnected architecture, with the 9:1 (ADAG: CNF, v/v) hydrogel exhibiting a more homogeneous and compact network structure, similar to ADAG. Optimization identifies 9:1 and 8:2 ratios as maintaining crosslinking density, while 7:3 ratio slightly disrupts uniformity but retains fast gelation (<5 min) and smooth injectability. CNF reinforcement markedly enhanced mechanical properties, as evidenced by increased storage modulus (0.007 MPa) and compressive modulus (0.006 MPa). The hydrogels exhibit high self-healing efficiency (98%) and support robust proliferation of human bone marrow-derived mesenchymal stem cells. Biochemical and gene-expression analyses show enhanced glycosaminoglycan and collagen deposition, upregulation of chondrogenic markers (SOX9, COL2A1, ACAN), and low COL1A1 expression. Overall, CNF-reinforced ADAG hydrogels combine cytocompatibility, mechanical resilience, injectability, and chondroinductive potential, highlighting suitability for stem cell-mediated cartilage tissue engineering applications. - Source: PubMed
Sudha AnjaliNatarajan AmritaMorris HarmonyHaynes AlyeriahVijayan Vineeth MMoore Roderquita KDean Derrick