Ask about this productRelated genes to: TNFAIP8 antibody
- Gene:
- TNFAIP8 NIH gene
- Name:
- TNF alpha induced protein 8
- Previous symbol:
- -
- Synonyms:
- GG2-1, MDC-3.13, SCC-S2
- Chromosome:
- 5q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-11
- Date modifiied:
- 2015-11-23
Related products to: TNFAIP8 antibody
Related articles to: TNFAIP8 antibody
- MicroRNA-155 (miR-155) is a crucial miRNA that connects inflammation signaling with epigenetic regulation, impacting programmed cell death (PCD) and influencing chemotherapy resistance. It inhibits apoptosis by targeting pro-apoptotic factors and adjusts autophagy via PDK1/AKT-mTOR activation or downregulating ATG5, helping cells cope with stress. In many solid and hematologic cancers, the predominant pattern involves promoting resistance, mainly through miR-155-5p-driven suppression of pro-apoptotic or checkpoint regulators, involving PI3K/AKT, NF-κB, and STAT3 pathways. Conversely, some studies indicate chemosensitizing or tumor-suppressive roles in specific contexts, such as miR-155-3p/MYD88 signaling in breast cancer, miR-155/XIAP in ovarian cancer, and miR-155/CD47-TNFAIP8 in multiple myeloma. miR-155 also influences autophagy depending on the context, either promoting protective autophagy by targeting mTOR pathway regulators or enhancing chemosensitivity by suppressing key autophagy components like ATG5. New findings associate miR-155 with pyroptosis, necroptosis, and immune clearance via phagocytosis, though the mechanisms vary across pathways. In the tumor microenvironment, exosomal miR-155 spreads resistance traits, such as epithelial-mesenchymal transition, stemness, and survival signaling in adjacent cells. Therapeutic approaches include inhibition or restoration, tailored to isoform, tumor type, and network, with growing support for oligonucleotide-based therapies, nanoparticle delivery, and combination treatments. Overall, miR-155 is a powerful biomarker for chemoresistance and a promising therapeutic target, especially when strategies are isoform- and context-specific. This review adopts a mechanism-first approach to distinguish common resistance modules from true context-dependent exceptions, highlighting isoform specificity and translational relevance. - Source: PubMed
Publication date: 2026/04/03
Abdul-Rahman Saeb YounisShareef AbdulkareemJyothi S RenukaNayak Priya PriyadarshiniJanney J BethanneySingh GurjantSinha AashnaTilyavova SitoraSameer Hayder NajiYaseen AhmedSalih Rasim MAdil Mohaned - Coronary artery disease (CAD), a chronic progressive inflammatory cardiovascular disorder and leading global cause of mortality, imposes a substantial worldwide economic burden. Identifying lipid metabolism-related genes linked to CAD is crucial for deepening our understanding of the disease's pathogenesis and discovering novel therapeutic targets. A total of 700 differentially expressed genes associated with CAD were determined by comparing CAD patients and healthy controls in the GSE250283 dataset. A positive relationship between lipid exposure and CAD was revealed by implementing a 2-sample Mendelian randomization analysis using genome-wide association studies data on lipid metabolism exposures and CAD outcomes. Further Mendelian randomization analysis, employing expression quantitative trait loci data from the identified differentially expressed genes as exposures and intersecting results with the Kyoto Encyclopedia of Genes and Genomes lipid metabolism pathway, identified 19 key genes exhibiting both lipid regulatory characteristics and reliable causal associations with CAD. Finally, 5 biomarker genes (SCP2, TNFAIP8, HMGCR, AGPAT3, and MAPKAPK2) were selected from the key genes by implementing 4 machine learning algorithms, and the developed nomogram incorporating these biomarkers demonstrated superior predictive accuracy for CAD risk stratification. The identification of these 5 genes as causal lipid metabolism biomarkers of CAD offers novel insights with high clinical potential, providing valuable targets for the management and treatment of CAD. - Source: PubMed
Bure QiSun WenjinWang LujiaoZhang XinShuang Lian - Hyperinsulinemia, a hallmark of obesity and type 2 diabetes, is an emerging risk factor for pancreatic ductal adenocarcinoma (PDAC), yet its contribution to tumor progression and stromal remodeling remains unclear. Here, we identify an insulin-exosome-TNFAIP8-STAT1 signaling axis that is associated with fibroblast phenotypic remodeling and desmoplastic progression. Insulin activates PI3K/AKT-RAB3A signaling to enhance secretion of TNFAIP8-enriched exosomes from PDAC cells. Internalized TNFAIP8 recruits the E3 ligase TRIM21 to facilitate STAT1 ubiquitination and degradation, leading to the induction of myofibroblastic CAF-associated features, accompanied by enhanced extracellular matrix deposition and tumor growth. High TNFAIP8 expression in patient tumors correlates with fibrosis and poor prognosis. In orthotopic models, TNFAIP8 silencing or lipid nanoparticle-mediated shTNFAIP8 delivery reduced fibrosis, suppressed tumor progression, and enhanced gemcitabine efficacy without evident toxicity, suggesting the feasibility of a therapeutic approach. These findings uncover a mechanistic framework linking metabolic dysregulation to fibroinflammatory remodeling in PDAC, and nominate TNFAIP8 as a promising stromal-targeted therapeutic candidate. - Source: PubMed
Publication date: 2026/02/19
Li ZhenyuChen LiWang TaoJiang HaiyangWang HuijuanLi MengyuXie GuanpengXi ChunhuaYan HanLu ChunhuiLi ChenchenZhu HanyuSun FeihuYin LingdiYu JunMiao Yi - Tumor necrosis factor-α-induced protein-8 (TNFAIP8/TIPE) like-2 (TIPE2), a critical member of the TIPE protein family, has been characterized as a tumor suppressor across multiple malignancies. Its functional significance in cholangiocarcinoma pathogenesis remains poorly defined. To address this knowledge gap, we established a discovery cohort of 218 cholangiocarcinoma patients and an independent validation cohort of 95 cases. The expression of TIPE2 was explored via immunohistochemistry (IHC). The correlation between patients' clinical parameters including overall survival and TIPE2 expression were evaluated. A nomogram including TIPE2 expression was also constructed and validated to for prognostic prediction. The effect and related mechanisms of TIPE2 on the malignant behaviors of cholangiocarcinoma was investigated both in vitro, in silico, and in vivo. The two cohorts demonstrated that TIPE2 expression was decreased in cholangiocarcinoma tissues, and TIPE2 expression was closely related with tumor stage and the prognosis of cholangiocarcinoma patients. Nomogram including TIPE2 expression could predict the prognosis of cholangiocarcinoma patients effectively. TIPE2 suppressed the proliferation, migration and invasion capacities of cholangiocarcinoma cells, and inhibited tumor growth in vivo. Mechanistically, TIPE2 suppressed the trafficking of integrin αvβ6 via targeting RAC1, which subsequently suppressed the progression of cholangiocarcinoma. Through comprehensive clinical cohorts and functional investigations, the present study identified TIPE2 as a clinically significant prognostic biomarker and revealed its potential role in regulating integrin-mediated oncogenic processes in cholangiocarcinoma. Therapeutic enhancement of TIPE2 expression emerges as a promising precision medicine strategy for cholangiocarcinoma management. - Source: PubMed
Publication date: 2026/01/29
Wang ShashaJia WenyuSun YuqiMeng ChengNiu JunLi Zequn - - Source: PubMed
Publication date: 2025/08/30
Tian ZuozhenChen KenShofer Frances SChenna Srish SSandroni Daniel ZQin LingZhang Yejia