ArticleCell death & disease2024
TRIM22 induces cellular senescence by targeting PHLPP2 in hepatocellular carcinoma.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Targeting PLD3 Reverses the Immunosuppressive Niche by Reprogramming Tumor-Associated Macrophages and Potentiates Antitumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Prolonged KRAS-MAPK Inhibition Induces Interferon Signaling That Promotes Cell State Transition and Confers Therapeutic Vulnerabilities.Cancer research · 2026Article
- Identification of potential biomarkers and therapeutic targets for liver cirrhosis based on Mendelian randomization and machine learning.Biochemistry and biophysics reports · 2026Article
- COMPASS subunit Bre2 regulates chromatin remodeler Arp9 to control Aspergillus flavus aflatoxin synthesis and virulence.Nature communications · 2026Article
- Induction of TRIM22 promotes autophagy and apoptosis of colorectal cancer through reactive oxygen species generation.Journal of translational medicine · 2026Article
- WWP2-induced inhibition of hepatocellular carcinoma cellular senescence via the ubiquitination and degradation of p21.Cell death & disease · 2025Article
- ATP6V0D2 drives triple-negative breast cancer progression and inhibits cisplatin sensitivity by promoting PHLPP2 lysosomal degradation.iScience · 2025Article
- Single-cell analysis revealed a diagnostic model of hepatocellular carcinoma based on cancer stem cell-related gene.Translational cancer research · 2025Article
- Hypomethylation-Enhanced F-Box Protein 32 Promotes Hepatocellular Carcinogenesis via Ubiquitin-Mediated PHLPP2 Degradation.MedComm · 2025Article
- TRIM22 mechanism promoting KAT2A ubiquitination degradation to regulate ferroptosis in hepatocellular carcinoma cell invasion and metastasis.Histology and histopathology · 2025Article
- Systematic analysis identifies TRIM22 as an oncogenic and immunological biomarker in glioma.BMC cancer · 2025Article
- E3 ligase TRIM22 promotes melanoma proliferation by regulating cell cycle progression through K63-linked ubiquitination of p21.Scientific reports · 2025Article
- ADRB2 is regulated by TRIM22 and facilitates lung adenocarcinoma progression via JAK2/STAT3 signaling pathway.Scientific reports · 2025Article
- TRIM22 governs tumorigenesis and protects against endometrial cancer-associated cachexia by inhibiting inflammatory response and adipose thermogenic activity.Cancer & metabolism · 2025Article
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- Identification of CCNB1 as a biomarker for cellular senescence in hepatocellular carcinoma: a bioinformatics and experimental validation study.Discover oncology · 2025Article
- Comprehensive analysis of PSMG3 in pan-cancer and validation of its role in hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- TRIM22 functions as a scaffold protein for autophagy initiation.Animal cells and systems · 2025Article
- PP2C phosphatases-terminators of suicidal thoughts.Cell death & disease · 2024Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
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Abstract
The ubiquitin-proteasome system is a vital protein degradation system that is involved in various cellular processes, such as cell cycle progression, apoptosis, and differentiation. Dysregulation of this system has been implicated in numerous diseases, including cancer, vascular disease, and neurodegenerative disorders. Induction of cellular senescence in hepatocellular carcinoma (HCC) is a potential anticancer strategy, but the precise role of the ubiquitin-proteasome system in cellular senescence remains unclear. In this study, we show that the E3 ubiquitin ligase, TRIM22, plays a critical role in the cellular senescence of HCC cells. TRIM22 expression is transcriptionally upregulated by p53 in HCC cells experiencing ionizing radiation (IR)-induced senescence. Overexpression of TRIM22 triggers cellular senescence by targeting the AKT phosphatase, PHLPP2. Mechanistically, the SPRY domain of TRIM22 directly associates with the C-terminal domain of PHLPP2, which contains phosphorylation sites that are subject to IKKβ-mediated phosphorylation. The TRIM22-mediated PHLPP2 degradation leads to activation of AKT-p53-p21 signaling, ultimately resulting in cellular senescence. In both human HCC databases and patient specimens, the levels of TRIM22 and PHLPP2 show inverse correlations at the mRNA and protein levels. Collectively, our findings reveal that TRIM22 regulates cancer cell senescence by modulating the proteasomal degradation of PHLPP2 in HCC cells, suggesting that TRIM22 could potentially serve as a therapeutic target for treating cancer.
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