TRIM47 (Tripartite Motif Containing 47)

CZ-2401 effectively stabilizes HNF4α protein in HCC cells and ameliorates TRIM47-driven HCC progression in vivo. Taken together, our research elucidates that targeting TRIM47-HNF4α interaction is a potential therapeutic strategy for HCC, and identifies CZ-2401 as a potent inhibitor of HNF4α degradation and a promising candidate for HCC therapy.

Rescue experiments and bortezomib intervention experiments further confirmed that FBP1 is essential for mediating the oncogenic effects of TRIM47 in HCC progression. To explore its therapeutic potential, TRIM47 siRNA was developed and loaded into poly (lactic acid)-DC-Chol nanoparticles (siTRIM47@PD NPs), which significantly reduced tumor growth and metastasis in an orthotopic HCC animal model, highlighting the potential of TRIM47 as a therapeutic target. Together, these findings underscore the pivotal role of TRIM47 in HCC progression through FBP1-mediated regulation of energy metabolism, and highlight siRNA-based TRIM47 targeting as a promising approach to improve HCC treatment outcomes.

On-going confirmation of the impact of endothelial and astrocytic autophagy with myelination will elucidate underlying mechanisms of sporadic AD progression. Understanding the role of autophagy of astrocytes may highlight additional factors affecting neurodegenerative disorders.

FH overexpression restored the effects of TRIM47. Collectively, the observations demonstrate that TRIM47 accelerates the progression of ICC by interacting with FH and ubiquitinating FH, indicating that TRIM47/FH axis may be potential target for ICC treatment.

Additionally, via Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA), we identified the disparities in its biological functions and signaling pathways and further investigated the relationship between immune infiltrations. In summary, the findings of this study may facilitate the discovery of novel therapeutic targets and prognostic biomarkers for UVM, thereby laying the foundation for the precision medicine of patients.

More notably, our in vivo assays showed that loss of TRIM47 slowed the growth rate of osteosarcoma xenograft tumours. Overall, our data indicated that TRIM47 facilitates OS progression by promoting proteasomal degradation of FBP1, thereby activating the Wnt/β-catenin pathway, which clarified that targeting the TRIM47-FBP1-β-catenin axis could be a promising approach for treating OS.

This review identifies TRIM proteins that are involved in urological cancers. Some of these proteins have the potential to be the therapeutic target.

Additionally, HRGECs were treated with the proteasome inhibitor MG132 to inhibit proteasome activity, thereby inhibiting the degradation of proteins via the ubiquitin-proteasome pathway, and found that MG132 effectively inhibited the degradation of SIRT1...Subsequently, TRIM47 interacted with SIRT1, facilitating its ubiquitination and subsequent degradation, thereby inhibited the deacetylation of HMGB1. This process resulted in the translocation of substantial quantities of AcHMGB1 from the cytoplasm to extracellular milieu, where it interacts with podocytes and induces apoptosis.

Comprehensively, glycogen synthase kinase-3β (GSK-3β)-associated ubiquitination is critical in the TRIM47-ADAR-GSK-3β axis. This study demonstrates that TRIM47 interacted with ADAR to facilitate ADAR protein degradation via ubiquitination and GSK-3β-associated phosphorylation, which serves as a novel therapeutic avenue for TC.

This enhanced TRAF2 Lys63 polyubiquitylation and induced nuclear factor (NF)-κB activation, leading to synovial hyperplasia and abnormal proliferation of FLSs. Our study provides a mechanistic and preclinical rationale for further evaluation of GRK2 as a therapeutic target for RA.

TRIM47 promoted paclitaxel resistance in ovarian cancer by inducing PPM1A degradation and activating the TGF-β pathway.