Ask about this productRelated genes to: TRIB3 antibody
- Gene:
- TRIB3 NIH gene
- Name:
- tribbles pseudokinase 3
- Previous symbol:
- C20orf97
- Synonyms:
- dJ1103G7.3, TRB3
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-10-05
Related products to: TRIB3 antibody
Related articles to: TRIB3 antibody
- Acquired drug resistance is a major cause of failure in gastric cancer treatment. The protein tyrosine phosphatase receptor type E (PTPRE) plays an oncogenic role in certain tumours; however, its function in chemotherapy-resistant gastric cancer remains unclear. Therefore, we analysed PTPRE expression in gastric cancer using The Cancer Genome Atlas. In vitro experiments were then conducted to investigate the effects of PTPRE on the resistance of cancer cells to 5-fluorouracil (5-FU) and its potential mechanisms. The results were further validated in vitro using xenograft studies. We found that PTPRE is upregulated in gastric cancer tissues and participates in the induction of 5-FU resistance. Mechanistic studies revealed that PTPRE suppressed ferroptosis in gastric cancer cells and promoted 5-FU resistance by activating the Src/FAK pathway to upregulate TRIB3 expression. In summary, PTPRE suppresses ferroptosis in gastric cancer cells via the Src/FAK/TRIB3 signalling pathway, thereby inducing 5-FU resistance. Intervention with PTPRE and its downstream targets may represent a potential approach for the clinical treatment of 5-FU-resistant gastric cancer. - Source: PubMed
Publication date: 2026/06/18
Liu MingLiao XiaomeiWang FangchaoJiao PengqingWang Zhongkai - Spermine oxidase (SMOX), a key enzyme in polyamine catabolism, has been increasingly linked to tumor progression. However, its regulatory network and biological significance in colorectal cancer (CRC), particularly in metastasis, remain largely undefined. Integrated transcriptomic analyses of CRC peritoneal metastasis samples, GEO datasets, and TCGA cohorts were performed to determine SMOX expression and prognostic value. Functional assays in vitro and xenograft/peritoneal metastasis models in vivo were used to assess the impact of SMOX knockdown or overexpression. Mechanistic studies included pathway enrichment, Western blotting, Co-IP, and ChIP-qPCR. SMOX was consistently upregulated in CRC tissues and cell lines, and high SMOX expression correlated with advanced stage, lymphatic metastasis, and unfavorable prognosis. Functionally, SMOX depletion markedly suppressed CRC cell proliferation, colony formation, migration, and invasion, and impaired tumor growth and peritoneal dissemination in vivo; SMOX overexpression exerted opposite protumorigenic effects. Mechanistically, SMOX elevated intracellular ROS levels, leading to transcriptional upregulation of the pseudokinase TRIB3. TRIB3 interacted with and suppressed GSK-3β activity, consequently stabilizing β-catenin and activating the Wnt/β-catenin pathway. Moreover, we identified ZNF263 as a previously unrecognized transcriptional activator of SMOX; ZNF263 directly bound to the SMOX promoter and drove its overexpression in CRC. Together, these findings delineate a novel "ZNF263-SMOX-ROS-TRIB3-GSK-3β-β-catenin" axis. Our study reveals SMOX as a critical driver of CRC progression and metastasis through ROS-mediated TRIB3 induction and subsequent Wnt/β-catenin activation, under the upstream regulation of ZNF263. This signaling axis provides new mechanistic insights and highlights SMOX/TRIB3 as promising therapeutic targets in CRC. - Source: PubMed
Publication date: 2026/06/09
Sun LongheZhang YouleiZhang XianhuZhou JiajieJi LiliLi RuiqiZhao ShuaiFu YayanWang JieTang MinWang WeiQian ChunhuaSun QiannanWang Daorong - Dengue virus (DENV) is responsible for hundreds of millions of infections per year, but no clinically approved antiviral therapy exists, and direct-acting candidates are limited by toxicity and viral genetic diversity. Traditional medicinal preparations such as Nimba/Neem (Azadirachta indica) and polyherbal Ayurvedic preparation Triphala (a combination of Terminalia chebula, Terminalia bellirica and Phyllanthus emblica) contain multiple metabolites with antiviral and antioxidant properties but their mechanisms of action are not fully characterised. Here, we combined cell-based antiviral assays with transcriptome profiling to compare how Nimba and Triphala shape host responses during DENV infection in RAW264.7 macrophages, a key innate immune target. Nimba and Triphala demonstrated low cytotoxicity in the concentrations of our assays, which supports a favourable therapeutic window. The RNA-seq analysis showed that Nimba induced broader transcriptional reprogramming in DENV-infected macrophages than Triphala, with 4,182 differentially expressed genes in the NB + DV versus DV comparison, indicating a stronger host transcriptional impact during infection. It increased interferon-stimulated gene (Isg15) programs and attenuated inflammatory signalling (e.g., Cxcl10), oxidative stress (Txnip, Aox4, Phlda3), and endoplasmic reticulum stress pathways (Trib3) upon infection. Triphala, in contrast, caused relatively restrained baseline transcriptional reprogramming and a more selective infection-context response. Docking analysis suggested that Triphala-associated metabolites may engage multiple DENV proteins. In line with this, molecular docking of nine proteins of DENV indicated multi-target binding of Triphala metabolites, with corilagin showing favorable predicted binding affinities (ΔG -13.9 kcal/mol), in certain proteins, superior to that of reference compounds (Remdesivir and NITD008). Together, these data support broader host-response modulation by Nimba and a more selective host response with a possible virus-directed contribution for Triphala during DENV infection and lay the foundational research for synthesis of anti-viral herbal formulations using Nimba and Triphala ingredients. - Source: PubMed
Publication date: 2026/06/05
Chakraborty DebayaniNamitha RRoy RahulDevi K Lavanya - In clear cell renal cell carcinoma (ccRCC), aberrant accumulation of hypoxia-inducible factor-2α (HIF-2α) due to VHL gene mutation is a central event driving tumorigenesis and progression. Although DNA damage is a hallmark of renal cancer development, it remains unclear whether and how HIF-2α regulates downstream targets to modulate the DNA damage and repair process. Here, we demonstrate that HIF-2α transcriptionally activates TRIB3 expression. Further we found that TRIB3 interacts with PARP1, a key DNA repair protein, and enhances nuclear PARP1 stability by inhibiting its K63-linked polyubiquitination, thereby promoting the DNA repair capacity of ccRCC cells. Both in vitro and in vivo, the HIF-2α inhibitor belzutifan (PT2977) effectively suppressed this signaling axis and reversed the tumor-promoting effects caused by PARP1 overexpression. Collectively, our findings elucidate a critical role for the HIF-2α/TRIB3/PARP1 axis in ccRCC progression, revealing potential therapeutic targets and rational combination strategies for this disease. - Source: PubMed
Publication date: 2026/06/03
Li WeiyiXu QiliSong JianSong WeijieFei MintianZhang KaipinYan Zejun - often acts as a negative regulator of lipid metabolism in the body, however, little is known about the effect of on milk lipid metabolism in YMECs. Therefore, we investigated the functional role of in lipid metabolism by transfecting YMECs with an overexpression vector and an interference vector. The results showed that after overexpression of , the mRNA expression levels of 10 genes related to milk fat metabolism in YMECs were very significantly downregulated ( < 0.01), the total triglyceride content was very significantly decreased ( < 0.001), lipid droplet accumulation was reduced, and the protein expression level of -Akt was very significantly decreased ( < 0.01). The downregulation of the above protein levels was weakened by the addition of the Akt phosphorylation agonist SC76. After interference with , the expression levels of 9 genes related to milk fat metabolism in YMECs were very significantly upregulated ( < 0.01), the total triglyceride content was very significantly increased ( < 0.01), lipid droplet accumulation was increased, and the protein expression levels of p-Akt ( < 0.01), PPARg ( < 0.05) and p-mTOR ( < 0.01) were very significantly upregulated. The upregulation of the above protein levels was reversed by the addition the Akt phosphorylation inhibitor MK2206. These results indicated that the gene negatively regulates lipid synthesis in YMECs. affects lipid metabolism by inhibiting Akt phosphorylation, which lays a theoretical foundation for further studies on lipid metabolism in YMECs and for improving yak milk quality. - Source: PubMed
Publication date: 2026/05/05
Zheng JialeLei FanLiu ShiangZhao YaqinZhang ZiyuDong BaoxiaFeng HuinaJing Haixia