Ask about this productRelated genes to: THOC3 Blocking Peptide
- Gene:
- THOC3 NIH gene
- Name:
- THO complex 3
- Previous symbol:
- -
- Synonyms:
- TEX1, MGC5469
- Chromosome:
- 5q35.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-09
- Date modifiied:
- 2016-10-05
Related products to: THOC3 Blocking Peptide
Related articles to: THOC3 Blocking Peptide
- The development of compounds triggering intestinal stem cells (ISCs) proliferation represents a promising strategy to alleviate irradiation (IR)-induced gastrointestinal syndrome. Here, cannabidiol (CBD)-a nonpsychotomimetic phytocannabinoid derived from the Cannabis sativa plant-was found to dramatically improve body weight loss of mice and stimulate Lgr5 ISCs proliferation upon a lethal dose of IR. Using absolute quantitative lipidomics, we found that the dysregulation of fatty acids in crypts induced by IR was rescued by CBD, which was indispensable for ISCs regeneration. Integrative analysis of transcriptome and lipidomics unveiled the critical role of PPARα in regulating fatty acid β-oxidation (FAO) by transcriptionally upregulating Slc27a2 and Acox1. Further experiments showed that CBD could trigger the enrichment of Stat2 on the promoter region of Pparα, ultimately facilitating the FAO program and subsequent ISCs proliferation following IR exposure. In addition,THOC3 was identified as a direct target of CBD, which stabilized the THOC3 protein and substantially alleviated the IR-induced blockade of Stat2 mRNA nuclear export. This study reveals a connection between CBD-driven ISCs proliferation and the FAO program during IR damage, providing a promising avenue for IR-induced gastrointestinal syndrome treatment. The binding of CBD to THOC3 maintains its radiation stability, which then supports the nuclear export of Stat2 mRNA for the subsequent transactivation of Pparα. The upregulation of PPARα will ultimately stimulate the FAO program, thereby facilitating ISCs regeneration during IR exposure. - Source: PubMed
Publication date: 2026/05/12
Liao ZebinHuang CongshuZhang LiangliangHu ChangkunWu ZekunBai ZhijieLi GaofuZhou LeiWang NingningHuangfu ChaojiNi ZhexinShen PanZhou WeiGao Yue - Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide. Although the transcription-export (TREX) complex plays a central role in RNA maturation and nuclear export, the clinical and biological relevance of individual THO Complex Subunit (including THOC1, THOC2, THOC3, THOC5, THOC6, and THOC7) in LUAD is not well defined. We performed integrative analyses combining bulk transcriptomics from TCGA/GTEx and independent GEO cohorts, survival modeling, DNA methylation profiling, protein-level annotation from public resources, protein-protein interaction network analysis, immune infiltration estimation (TIMER), and single-cell RNA sequencing (scRNA-seq) to evaluate the relevance of THOC3 and THOC7 in LUAD. Across TCGA and external GEO validation datasets, THOC3 and THOC7 were consistently upregulated in LUAD and associated with poorer overall and disease-free survival, whereas other THO complex members showed weaker or inconsistent associations. Given these comparatively consistent and reproducible signals, we therefore prioritized THOC3 and THOC7 for downstream multi-layer analyses. Epigenetic profiling and interaction network analyses placed both genes within conserved RNA processing and export programs linked to genome maintenance pathways. Single-cell transcriptomic analysis provided additional resolution, demonstrating predominant enrichment of THOC3 and THOC7 in malignant epithelial clusters, with THOC3 aligning with transcriptional programs associated with DNA replication and repair, and THOC7 with proliferative and checkpoint-related states. Notably, expression of both genes was also detectable in myeloid and neutrophil subsets, and THOC7 expression remained elevated in recurrent LUAD samples, indicating association with aggressive and treatment-resistant disease states. Collectively, by integrating bulk, single-cell, epigenetic, and immune profiling across multiple independent cohorts, this study identifies THOC3 and THOC7 as reproducible molecular correlates of aggressive LUAD phenotypes. These highlight dysregulated RNA export programs as potential biomarkers of poor prognosis and motivate future functional studies to assess RNA export dependencies in LUAD. - Source: PubMed
Publication date: 2026/03/09
Kumar SachinWu Chung-CheSolomon Dahlak DanielYen Meng-ChiYeh I-JengKo Ching-ChungXuan Do Thi MinhChang Kai-FuLin Hui-RuLin Hung-YunShih Chia-LungChen Jian-BinLee Wei-YiWang Chih-YangLee Yung-KuoNguyen Ngoc Uyen Nhi - Located on chromosome 5, the THOC3 gene encodes a protein of 351 amino acids, though its precise biological role in various malignancies, including lung cancer (LC), remains to be fully clarified. Elevated expression of THOC3 was observed in LC (IHC) analyses. Increased THOC3 levels were associated with advanced tumor stages and poorer prognosis in patients. Functional studies using both loss-of-function and gain-of-function approaches suggested that THOC3 may influence cellular proliferation, tumorigenic potential, and apoptosis in vitro. Mechanistically, its effects appear to involve activation of the STAT3 pathway. Additionally, Garcinone d-induced STAT3 activation mitigated certain malignant characteristics of LC cells, though silencing THOC3 reversed this effect. These results indicate that THOC3 may serve as a potential prognostic marker and could warrant further investigation as a therapeutic target in LC. - Source: PubMed
Publication date: 2026/03/22
Ni ZhengzhengZhou ShengZhang YanWang XinyangYang HuiZhou HanyuTao Zheng - The intestinal epithelium possesses a profound capacity for regeneration, which is fueled by the proliferation and differentiation of leucine-rich repeat-containing G-protein-coupled receptor 5 (Lgr5)-expressing intestinal stem cells (ISCs) located at the base of the crypts. However, how small nucleolar RNAs (snoRNAs) regulate the self-renewal of ISCs remains elusive. Here, we identified a small nucleolar RNA Snord17 that is highly expressed in ISCs. Snord17 knockout abrogates stemness of ISCs and impairs epithelial regeneration. Mechanistically, Snord17 interacts with THO complex 3 (Thoc3) to facilitate nuclear export of Yin yang 2 transcription factor (Yy2) mRNA for its subsequent translation. Yy2 protein enriches on the promoter of TEA domain family member 4 (Tead4) to activate its transcription, leading to activation of Hippo signaling for self-renewal maintenance of ISCs. Of note, Tead4 deficiency impairs self-renewal of ISCs and intestinal regeneration. Our findings reveal that the Snord17-Thoc3-Yy2-Tead4 axis is required for self-renewal maintenance of ISCs and gut regeneration. - Source: PubMed
Publication date: 2026/01/04
Zhang PeikangXu YuweiLan YufeiXiong ZhenYi ZhibinWu RunyuanLi CunzhenDu YingGuo HuiYang YingchiFan Zusen - There is a Limited number of studies on THO Complex Subunit 3 (THOC3) in tumors. The purpose of this study is to conduct a comprehensive analysis of various types of tumors to determine the role of THOC3 in tumor progression and to investigate its impact on immunity. Retrieved THOC3 expression data from various cancers in the TCGA database and analyzed it using R software (version 3.6.4) and its related packages; explored the differential expression of THOC3 in tumors, its correlation with prognosis, functional enrichment, and its relationship with tumor heterogeneity. The study also aimed to uncover the correlation between THOC3 and tumor immunity. THOC3 is differentially expressed in various tumors and normal samples, and is correlated with overall survival and progression-free time. The study found that THOC3 expression is strongly associated with tumor mutational burden, microsatellite deletion, and immune response. The expression of THOC3 is significantly correlated with immune cell infiltration, and THOC3 can regulate transcription output and mRNA splicing. Therefore, we speculate that THOC3 could serve as a therapeutic target for future anticancer therapies. THOC3 can serve as a novel specific biomarker for diagnosis and prognosis in pan cancer. - Source: PubMed
Publication date: 2025/10/16
Zhao QiZhang JixinCui XingZhao JidongChen Xin