ArticleCell communication and signaling : CCS2024
ZMAT2 condensates regulate the alternative splicing of TRIM28 to reduce cellular ROS accumulation, thereby promoting the proliferation of HCC cells.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TRIM28-Derived Peptide Exerts Anti-Tumor Roles by Stabilizing Tumor Suppressive BRD7 Protein in Multiple Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Risk model of liquid-liquid phase separation-related genes reveals the prognosis and tumor microenvironment characteristics of colorectal cancer.Journal of cell communication and signaling · 2025Article
- Contrasting Impacts of Targeted Disruption of the Cancer Stem Cell Marker CD133 and Its Epigenetic Regulator TRIM28 in Colorectal Cancer Cells.International journal of molecular sciences · 2025Article
- Integrated bioinformatics and experimental analysis of mitochondrial-associated membrane function and mechanism in acute respiratory distress syndrome.Scientific reports · 2025Article
- Targeting super-enhancers in liver cancer: from pathogenic mechanisms to clinical applications.Frontiers in pharmacology · 2025Review
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Authors and funding
16 authors.
Funding
Abstract
Dysregulation of splicing factor expression plays a crucial role in the progression of hepatocellular carcinoma (HCC). Our research found that the expression level of splicing factor ZMAT2 was increased in HCC, promoting the proliferation of HCC cells. RNAseq data indicated that the absence of ZMAT2 induced skipping exon of mRNA, while RIPseq data further revealed the mRNA binding motifs of ZMAT2. A comprehensive analysis of RNAseq and RIPseq data indicateed that ZMAT2 played a crucial role in the maturation process of TRIM28 mRNA. Knocking down of ZMAT2 led to the deletion of 25 bases in exon 11 of TRIM28, ultimately resulting in nonsense-mediated decay (NMD). Our data revealed that ZMAT2 could regulate TRIM28 to reduce the accumulation of ROS in HCC cells, thereby promoting their proliferation. Our research also discovered that ZMAT2 was capable of undergoing phase separation, resulting in the formation of liquid droplet condensates within HCC cells. Additionally, it was found that ZMAT2 was able to form protein-nucleic acid condensates with TRIM28 mRNA. In summary, this study is the first to reveal that ZMAT2 and TRIM28 mRNA form protein-nucleic acid condensates, thereby regulating the splicing of TRIM28 mRNA. The increased expression of ZMAT2 in HCC leads to upregulated TRIM28 expression and reduced ROS accumulation, ultimately accelerating the proliferation of HCC cells.
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