Ask about this productRelated genes to: TRIP6 Blocking Peptide
- Gene:
- TRIP6 NIH gene
- Name:
- thyroid hormone receptor interactor 6
- Previous symbol:
- -
- Synonyms:
- ZRP-1, OIP1, MGC10556, MGC10558, MGC29959, MGC3837, MGC4423
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2016-10-05
Related products to: TRIP6 Blocking Peptide
Related articles to: TRIP6 Blocking Peptide
- Hypoxia is a key feature of the tumor microenvironment in colorectal cancer (CRC), but the mechanisms linking hypoxia to metastasis remain incompletely understood. To investigate this, bioinformatics analysis of The Cancer Genome Atlas (TCGA) and Clinical Proteomic Tumor Analysis Consortium (CPTAC) datasets assessed TAR DNA-binding protein 43 (TDP-43) expression and its correlation with hypoxia-inducible factor-1α (HIF1A). In vitro and in vivo functional assays, including Cell Counting Kit-8 (CCK-8), Transwell, chicken chorioallantoic membrane (CAM), and xenograft, were conducted to evaluate proliferation, migration, invasion, and angiogenesis. Mechanistic studies, including chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), luciferase reporter, and actinomycin D assay, were conducted to elucidate HIF1-mediated transcriptional regulation of TARDBP and TDP-43-dependent stabilization of thyroid receptor-interacting protein 6 (TRIP6) mRNA. As a result, TDP-43 was upregulated in CRC tissues and correlated with HIF1A expression. Hypoxia induced TDP-43 expression through HIF1-dependent transcriptional activation via direct binding to hypoxia-response element (HRE) 3 site in the TARDBP promoter. TARDBP knockdown suppressed hypoxia-induced proliferation, migration, invasion, and vascular endothelial growth factor (VEGF) secretion, which were rescued by HIF1A overexpression. RIP-qPCR revealed TDP-43 binding to TRIP6 mRNA via its RNA recognition motifs (RRM domains), stabilizing TRIP6 transcripts and promoting its expression. TRIP6 reconstitution reversed the anti-tumor effects of TARDBP silencing. In vivo, TARDBP depletion inhibited tumor growth and downregulated metastasis-related factors in xenograft models. In conclusion, the HIF1-TARDBP-TRIP6 axis promotes CRC malignancy under hypoxia by integrating transcriptional activation and post-transcriptional mRNA stabilization, offering potential therapeutic targets for advanced CRC. - Source: PubMed
Publication date: 2026/06/12
Cheng KeLiu YonggangFeng WeiyuXu DongliHao Bin - TFEB (transcription factor EB) regulates the expression of autophagy and lysosomal genes, is activated by various cellular stresses, and plays a key role in maintaining cellular homeostasis. Recent work demonstrates that TFEB is activated during lysosomal damage through two distinct mechanisms: ATG conjugation-dependent and -independent. TFEB activation proceeds sequentially through two modes. In the early ATG conjugation-independent mode (Mode I), APEX1 interacts with TFEB in the nucleus, maintaining its transcriptional activity and protein stability. In the later ATG conjugation-dependent mode (Mode II), CCT7 and TRIP6 translocate to lysosomes and interact with TFEB, modulating its phosphorylation and nuclear localization. Moreover, TFEB regulation induced by other cellular stresses-such as oxidative stress, proteasome inhibition, mitochondrial damage, and DNA damage-also involves either Mode I or Mode II. Our findings provide new insights into a unified understanding of TFEB regulation under diverse cellular stress conditions. - Source: PubMed
Publication date: 2026/03/30
Shima TakayukiNakamura Shuhei - Smoking is a preventable cause of colorectal cancer (CRC), and nicotine metabolism may promote tumorigenesis. We aimed to investigate the prognostic significance of nicotine metabolism‑related genes (NRGs) in colon adenocarcinoma (COAD) and to develop a gene signature for patient stratification. - Source: PubMed
Publication date: 2026/02/11
Li JunliangZhang JunyiWang DanningShen JieyiShen ChongZeng WeiqiWang Jianwei - Pancreatic cancer (PC) is a leading cause of cancer-related mortality due to late diagnosis and limited treatments. Disulfidptosis, a novel form of regulated cell death, is implicated in disease pathogenesis. This study explores disulfidptosis-related gene (DRG) signatures to identify prognostic biomarkers and immune infiltration patterns in PC using bioinformatics and single-cell analyses. - Source: PubMed
Publication date: 2026/01/27
Pei YueCheng MeijiaYu TongMa WenjingSun XiaohanZhang JingyanLi JiajiaLi WenkaiZhou YutongHu HewenQi YingchaoLiu YunenWang Yichen - The clinical heterogeneity of colon adenocarcinoma (COAD) complicates patient prognosis and treatment. While metabolic reprogramming is a key driver of tumor progression, the role of histidine metabolism in the COAD immune microenvironment remains unclear. - Source: PubMed
Publication date: 2025/12/08
Zhong HuaJin JiangdongZhang YiChen NuoLiu AnyaJiang ChenfeiZhang WenbingHe Zirui