STAT3
- Known as:
- STAT3
- Catalog number:
- RP17131630010
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- STAT3
Related genes to: STAT3
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT3
Acpin1,Acrosomal protein ACPIN1,Mouse,Mus musculus,Sipar,STAT3-interacting protein as a repressorAnserine Signal Transducer And Activator Of Transcription 3 Elisa Kit (STAT3)Anserine anti - Signal Transducer And Activator Of Transcription 3 Elisa Kit (STAT3)Anti- STAT3 (Ab-705) AntibodyAnti- STAT3 (Ab-705) AntibodyAnti- STAT3 (Ab-727) AntibodyAnti- STAT3 (Ab-727) AntibodyAnti- STAT3 (Phospho-Ser727) AntibodyAnti- STAT3 (Phospho-Ser727) AntibodyAnti- STAT3 (Phospho-Tyr705) AntibodyAnti- STAT3 (Phospho-Tyr705) AntibodyAnti-Human STAT3, Rabbit PolyclonalAnti-Human STAT3, Rabbit Polyclonal affinity purified IgGanti-n STAT3 , Rabbit polyclonal to n STAT3 , Isotype IgG, Host RabbitAnti-phospho-STAT3 (pTyr705<_SUP>) produced in rabbit Antibody Related articles to: STAT3
- Bioactivation and clearance of anticancer agents are crucial factors in the efficacy and toxicity of anticancer drugs. Exosomes are membrane-bound vesicles secreted by tumor cells and the tumor microenvironment. These vesicles contain drug-metabolizing enzymes, transporters, and RNA. Exosomes can be non-invasively collected from the blood. This article has been prepared by combining the evidence of the role of exosomal cytochrome P450 isoforms, such as cytochrome P450 family 2 subfamily C member 19, cytochrome P450 family 2 subfamily D member 6, and cytochrome P450 family 3 subfamily A member 5, in the oxidation of anticancer drugs in the first phase of drug metabolism. Exosomal UDP-glucuronosyltransferase 1A1 has been found to help in the conjugation of anticancer drugs in the second phase of drug metabolism. Exosomal ATP-binding cassette transporters, P-glycoprotein, multidrug resistance-associated protein 1, and breast cancer resistance protein have been found to act as intercellular conveyors of drug efflux capacity. These transporters can modulate the efficacy of chemotherapy. Exosomal microRNAs, such as microRNA-21, microRNA-155, and microRNA-1246, have been found to modulate apoptosis, DNA repair, metabolic adaptation, and chemotherapy resistance through the PI3K/AKT pathway, EZH2/STAT3 pathway, and PDCD4 pathway. Long non-coding RNAs, such as UCA1 and HOXA antisense RNA, can reprogram the chromatin structure. These long non-coding RNAs can suppress tumor suppressor genes, thus leading to chemotherapy resistance. Bioinformatics pipelines have been designed to bridge the gap between exosomal RNA and protein levels in the profile of dynamic metabolic states. The challenges in the field of exosomal therapy drug monitoring have been discussed in the article. The article has recommended the use of artificial intelligence in the integration of omics with microfluidic technology for the improvement of exosomal therapy drug monitoring. - Source: PubMed
Satheesh SSekar VKaarnika V SMaageswaree B SBhoopendra G KIbrahim BNithish SGowtham V - Glioblastoma (GBM) is an aggressive brain tumor with limited treatment options and poor patient survival. This study aimed to identify key genes and altered pathways in GBM and to explore potential drug-repurposing candidates using a systems biology approach. - Source: PubMed
Publication date: 2026/09/08
Zaker ErfanNouri NegarPashangeh ParsaDizaji Saeid RazaviAsghari RahimDavoodi AkbarRahimmanesh Ilnaz - Hepatocellular carcinoma is the sixth most common cancer worldwide and a leading cause of cancer related mortality. Risk factors include chronic hepatitis B/C, obesity, alcohol abuse, diabetes and metabolic disorders. In advanced stages, normal treatments such as surgery, transplantation and chemotherapy are not as effective as tumors develop resistance and do not target oncogenic pathways well. Small interfering RNA (siRNA) therapeutics have the potential to change treatment paradigms by silencing specific biological pathways, thus suppressing tumor progression. Polymeric nanoparticles (PNPs) such as poly(lactic-co-glycolic acid) (PLGA), polyethyleneimine (PEI) and stimuli-responsive copolymers have attracted attention as effective delivery systems for siRNA. These carriers protect siRNA from enzymatic degradation and facilitate its cellular uptake. Furthermore, the surface of the carriers can be modified with targeting ligands, eg, galactose or ASGPR antibodies, to improve tumor-specific delivery. The PNPs can be tuned to change their physical and chemical properties, are more stable and responsive to signals from the tumor microenvironment for regulated release. This means they perform better than lipophilic or metallic carriers. Hepatocyte specific absorption pathways even enhance the liver tropism. This review focuses on recent advances in siRNA based therapeutic strategies against hepatocellular carcinoma, with a special focus on PNPs mediated drug delivery systems. It describes significant oncogenic pathways like β-catenin and STAT3 and formulation techniques including nanoprecipitation and layer by layer assembly. The review also reports the increasing importance of artificial intelligence in siRNA design, formulation optimization, and personalized therapeutic methods to improve the clinical applicability of HCC treatment. - Source: PubMed
Publication date: 2026/10/01
Thalij Karkaz MYou Huay WoonHabeeb MohammadRatchagar Joan VijethaKhot Vidyarani SujitkumarGorde Prasad Laxman - Diabetic bone defects are difficult to repair because chronic hypoxia, oxidative stress, persistent inflammation, and impaired osteoangiogenic coupling disrupt the healing cascade. Here, we report a pH-responsive polysaccharide hydrogel, GOZ6, for spatiotemporally coordinated diabetic bone regeneration. GOZ6 is formed by dynamic Schiff base crosslinking between gelatin and oxidized konjac glucomannan and co-delivers ZIF-8@CaO and 6-gingerol, integrating gated oxygen release, calcium ion delivery, antioxidative protection, and immunomodulation. The hydrogel exhibited rapid gelation within approximately 67 s, a porous architecture with a porosity of 75.78%, pH-responsive degradation, and sustained oxygen release for up to 14 d under physiological conditions. Under mildly acidic conditions, approximately 60% of 6-gingerol was released within the first 3 d, supporting early anti-inflammatory and antioxidative intervention. In vitro, GOZ6 maintained cell viability above 90%, promoted macrophage polarization toward a reparative phenotype, suppressed pro-inflammatory cytokine production, and restored oxidative metabolism. Transcriptomic and protein analyses find that JAK1-STAT3 and PI3K-AKT may serve as central pathways involved in these effects. Moreover, the GOZ6-conditioned immune microenvironment enhanced endothelial migration and tube formation, alleviated oxidative stress in bone marrow mesenchymal stem cells, restored mitochondrial function, and promoted osteogenic differentiation. In a diabetic rat calvarial defect model, GOZ6 markedly enhanced vascularized bone regeneration, collagen deposition, and osteogenic marker expression while reducing local inflammation, without evident systemic toxicity. GOZ6 therefore provides a multifunctional strategy for converting diabetic bone defects into a repair-permissive microenvironment. - Source: PubMed
Publication date: 2026/10/05
Sun HaifuLv NanningDong HeGeng WeiShi JingWu XinhuiLi YonggangChen YuLu HaowenDai JunZheng LongpoQiao Yusen - Drug resistance significantly limits the long-term effectiveness of targeted therapies in lung cancer. AXL, a receptor tyrosine kinase (RTK), is a well-established driver of drug resistance in many cancers, including lung cancer. Epithelial cell adhesion molecule (EpCAM), which is commonly overexpressed in epithelial cancers, is also a critical signaling molecule. In this study, we elucidated the role of EpCAM in drug resistance and its mechanistic association with AXL. We found that soluble epithelial cell adhesion molecule (sEpCAM) expression robustly enhanced hallmark cancer phenotypes and promoted pro-survival functions by upregulating AXL expression. Gene expression and pathway analyses further identified significant alterations in core cancer signaling pathways, including NF-kB, STAT3, AKT, and ERK. The ectopic expression of sEpCAM concurrently upregulated endogenous EpCAM expression in the tumor environment. Functionally, sEpCAM confers broad resistance to conventional chemotherapy. Drug sensitivity assays revealed that proteasome inhibition effectively reversed the sEpCAM-induced drug resistance by reducing AXL protein levels. Translational analysis of the lung cancer patient cohort data indicated that patients with aggressive disease co-expressing EpCAM and AXL may be particularly amenable to proteasome-based therapy. Characterization of the EpCAM-AXL axis gene signature further uncovered connections to p53, integrin, and Rho GTPase signaling as well as an intriguing link to tumor immune evasion. Our findings suggest that EpCAM-AXL co-expression in a subset of patients with lung cancer serves as both a predictive biomarker and a promising therapeutic target to counteract treatment failure. - Source: PubMed
Publication date: 2026/10/06
Guerrero-Alba AlexaShacker MarkFleming Timothy PSmith Michael ABremner Ross MSankpal Narendra V