ArticleCell biology and toxicology2024
Activation of CTU2 expression by LXR promotes the development of hepatocellular carcinoma.
Article in Cell biology and toxicology, 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, 3 citations in OpenAlex.
- Rare Biallelic CTU2 Variants in an Individual With CAKUT: Clinical Characterization and Minigene Splicing Analysis.Molecular genetics & genomic medicine · 2026Article
- Role of liver X receptors in the pathogenesis and treatment of chronic liver disease (Review).Molecular medicine reports · 2026Review
- Novel Shared Heritable Candidate Risk Loci of Breast and Endometrial Cancer-A Swedish Haplotype Genome-Wide Association Study.International journal of molecular sciences · 2025Article
- Pan-cancer analysis identifies tRNA modification enzyme CTU2 as a novel tumor biomarker and its role in immune microenvironment.Frontiers in immunology · 2025Article
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
Cytosolic thiouridylase 2 (CTU2) is an enzyme modifying transfer RNAs post-transcriptionally, which has been implicated in breast cancer and melanoma development. And we found CTU2 participated in hepatocellular carcinoma (HCC) progression here. HepG2 cells as well as xenograft nude mice model were employed to investigate the role of CTU2 in HCC development in vitro and in vivo respectively. Further, we defined CTU2 as a Liver X receptor (LXR) targeted gene, with a typical LXR element in the CTU2 promoter. CTU2 expression was activated by LXR agonist and depressed by LXR knockout. Interestingly, we also found CTU2 took part in lipogenesis by directly enhancing the synthesis of lipogenic proteins, which provided a novel mechanism for LXR regulating lipid synthesis. Meanwhile, lipogenesis was active during cell proliferation, particularly in tumor cells. Reduction of CTU2 expression was related to reduced tumor burden and synergized anti-tumor effect of LXR ligands by inducing tumor cell apoptosis and inhibiting cell proliferation. Taken together, our study identified CTU2 as an LXR target gene. Inhibition of CTU2 expression could enhance the anti-tumor effect of LXR ligand in HCC, identifying CTU2 as a promising target for HCC treatment and providing a novel strategy for the application of LXR agonists in anti-tumor effect.
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