TRIM34

Last update 08 May 2025

Basic Info

Synonyms

IFP1, Interferon-responsive finger protein 1, RING finger protein 21

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Introduction

Functions as antiviral protein and contributes to the defense against retroviral infections (PubMed:17156811, PubMed:32282853). Acts as a capsid-specific restriction factor with the help of TRIM5 and prevents infection from non-host-adapted retroviruses (PubMed:32282853). During influenza A virus infection, promotes programmed cell death by targeting ZBP1 for 'Lys-63'-linked polyubiquitination (PubMed:35065966). In turn, promotes ZBP1 recruitment of RIPK3 to mediate virus-induced programmed necrosis (PubMed:35065966). Negatively regulates the function of mitochondria by enhancing mitochondrial depolarization leading to cytochrome c release and mitochondria-dependent apoptosis (PubMed:31956709). Promotes also the formation of multinucleated giant cells by means of cell fusion and phagocytosis in epithelial cells (PubMed:31487507).

100 Clinical Results associated with TRIM34

100 Translational Medicine associated with TRIM34

0 Patents (Medical) associated with TRIM34

Literatures (Medical) associated with TRIM34

01 Dec 2024·Journal of Biochemical and Molecular Toxicology

Interferon Induced Upregulation of Tripartite Motif 34 (TRIM34) Leads Apoptotic Cell Death in Lung Adenocarcinoma

Article

Author: Vasu, Vihas T. ; Golani, Aparna ; Shaikh, Afridi ; Nagariya, Nidhi ; Roy, Hetal ; Chaudhari, Kaushalkumar

ABSTRACTDespite breakthroughs in our understanding of lung cancer risk, development, immunologic control, and therapy choices, it remains one of the leading causes of cancer mortality. This study aimed to investigate the role of TRIM34 upon treatment of Interferon Gamma (IFN‐γ) in Non‐Small Cell Lung Cancer (NSCLC). NCI‐H23 cells were exposed to IFN‐γ in a dose‐ and time‐dependent manner to understand TRIM34 expression and its role as a co‐regulator of treatment. The regulatory role of TRIM34 on IFN‐γ exposure was studied by qRT‐PCR, Western blot analysis, immunocytochemistry, apoptosis assay and scratch assay. On exposure to IFN‐γ, TRIM34 expression at transcript and protein level was significantly upregulated. With its upregulation, NCI‐H23 underwent apoptosis and its rate of proliferation was impeded. Our results suggest that induction of TRIM34 by IFN‐γ treatment may lead to an anti‐tumor inflammatory response, resulting in NSCLC regression via apoptosis.

01 Jul 2024·Cancer Letters

CRISPR/Cas9 screen reveals that targeting TRIM34 enhances ferroptosis sensitivity and augments immunotherapy efficacy in hepatocellular carcinoma

Article

Author: Dai, Xinzheng ; Zhou, Suiqing ; Chen, Yining ; Xu, Jiali ; Tie, Xiaofeng ; Baheti, Tasiken ; Yang, Nanmu ; Yao, Feifan ; Huang, Wei ; Qian, Xiangjun ; Wang, Xuehao ; Zhang, Ruizhi ; Hao, Xiaopei ; Li, Qing ; Zhang, Liren ; Xu, Jing ; Yu, Kai ; Zhang, Yu

Hepatocellular carcinoma (HCC) is a prevalent malignancy characterized by complex heterogeneity and drug resistance. Resistance to ferroptosis is closely related to the progression of HCC. While HCC tumors vary in their sensitivity to ferroptosis, the precise factors underlying this heterogeneity remain unclear. In this study, we sought to elucidate the mechanisms that contribute to ferroptosis resistance in HCC. Whole-genome CRISPR/Cas9 screen using a subtoxic concentration (IC20) of ferroptosis inducer erastin in the HCC cell line Huh7 revealed TRIM34 as a critical driver of ferroptosis resistance in HCC. Further investigation revealed that TRIM34 suppresses ferroptosis in HCC cells, promoting their proliferation, migration, and invasion both in vitro and in vivo. Furthermore, TRIM34 expression is elevated in HCC tumor tissues, correlating with a poor prognosis. Mechanistically, TRIM34 directly interacts with Up-frameshift 1 (UPF1), a core component of the nonsense-mediated mRNA decay (NMD) pathway, to promote its ubiquitination and degradation. This interaction suppresses GPX4 transcript degradation, thus promoting the protein levels of this critical ferroptosis suppressor in HCC. In light of the close crosstalk between ferroptosis and the adaptive immune response in cancer, HCC cells with targeting knockdown of TRIM34 exhibited an improved response to anti-PD-1 treatment. Taken together, the TRIM34/UPF1/GPX4 axis mediates ferroptosis resistance in HCC, thereby promoting malignant phenotypes. Targeting TRIM34 may thus represent a promising new strategy for HCC treatment.

05 Apr 2024·Mediators of Inflammation

Potential Association of Gut Microbial Metabolism and Circulating mRNA Based on Multiomics Sequencing Analysis in Fetal Growth Restriction

Article

Author: Peng, Jing ; Tang, Hui ; Zhang, Xian ; Yang, Weitao ; Li, Hanmei ; Li, Dan

Objective. Fetal growth restriction (FGR) is a significant contributor to negative pregnancy and postnatal developmental outcomes. Currently, the exact pathological mechanism of FGR remains unknown. This study aims to utilize multiomics sequencing technology to investigate potential relationships among mRNA, gut microbiota, and metabolism in order to establish a theoretical foundation for diagnosing and understanding the molecular mechanisms underlying FGR. Methods. In this study, 11 healthy pregnant women and nine pregnant women with FGR were divided into Control group and FGR group based on the health status. Umbilical cord blood, maternal serum, feces, and placental tissue samples were collected during delivery. RNA sequencing, 16S rRNA sequencing, and metabolomics methods were applied to analyze changes in umbilical cord blood circulating mRNA, fecal microbiota, and metabolites. RT-qPCR, ELISA, or western blot were used to detect the expression of top 5 differential circulating mRNA in neonatal cord blood, maternal serum, or placental tissue samples. Correlation between differential circulating mRNA, microbiota, and metabolites was analyzed by the Spearman coefficient. Results. The top 5 mRNA genes in FGR were altered with the downregulation of TRIM34, DEFA3, DEFA1B, DEFA1, and QPC, and the upregulation of CHPT1, SMOX, FAM83A, GDF15, and NAPG in newborn umbilical cord blood, maternal serum, and placental tissue. The abundance of Bacteroides, Akkermansia, Eubacterium_coprostanoligenes_group, Phascolarctobacterium, Parasutterella, Odoribacter, Lachnospiraceae_UCG_010, and Dielma were significantly enriched in the FGR group. Metabolites such as aspartic acid, methionine, alanine, L-tryptophan, 3-methyl-2-oxovalerate, and ketoleucine showed notable functional alterations. Spearman correlation analysis indicated that metabolites like methionine and alanine, microbiota (Tyzzerella), and circulating mRNA (TRIM34, SMOX, FAM83A, NAPG) might play a role as mediators in the communication between the gut and circulatory system interaction in FGR. Conclusion. Metabolites (METHIONINE, alanine) as well as microbiota (Tyzzerella) and circulating mRNA (TRIM34, SMOX, FAM83A, NAPG) were possible mediators that communicated the interaction between the gut and circulatory systems in FGR.

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TRIM34

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