ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
TRIM38 Suppresses the Progression of Colorectal Cancer via Enhancing CCT6A Ubiquitination to Inhibit the MYC Pathway.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- α-Hederin Alleviates Endoplasmic Reticulum Stress by Upregulating TRIM38 Expression, Thereby Inhibiting Hepatic Stellate Cell Activation and Liver Fibrosis.Biomedicines · 2026Article
- Chaperonin in health and disease.Molecular biomedicine · 2026Review
- TRIM38 Suppresses Breast Cancer Progression via Modulating SQSTM1 Ubiquitination and Autophagic Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrative single-cell and bulk transcriptomics define polyamine-associated cell states in acute myeloid leukemia and implicate CCT6A in polyamine homeostasis.Frontiers in immunology · 2026Article
- Tetrahydromagnolol targets TRIM38 to mediate PANoptosis in cancer cells and has the potential for synergistic cancer therapy.Experimental hematology & oncology · 2025Article
- Development of a recurrence-related gene signature and functional role of MLLT6 in ovarian cancer progression and Paclitaxel resistance.Journal of ovarian research · 2025Article
- TRIM38 Suppresses the Progression of Colorectal Cancer via Enhancing CCT6A Ubiquitination to Inhibit the MYC Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Emerging evidence reveals the pivotal function of tripartite motif protein (TRIM) in colorectal cancer (CRC). However, the precise function of TRIM38 and its underlying mechanism in CRC remains to be elucidated, especially regarding its putative ubiquitination function. Here, it is identified that TRIM38 is downregulated in CRC tissues by DNA hypermethylation of its promoter. Further analysis demonstrates that decreased TRIM38 is correlated with unfavorable clinical features and poor prognosis. Moreover, TRIM38 functions as a tumor suppressor by inhibiting cell proliferation, metastasis, and AOM/DSS-induced tumorigenesis in CRC cells. Mechanistically, TRIM38 binds to the substrate protein CCT6A, leading to the degradation and K48-linked ubiquitination of CCT6A at the K127/K138 residues. The elevation of CCT6A protein level caused by TRIM38 downregulation diminishes the degradation of c-Myc protein, thereby activating the MYC pathway. The study elucidates a novel mechanism of TRIM38/CCT6A/c-Myc axis regulating CRC, potentially offering a new therapeutic target for its treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.