TRIM4 (Tripartite Motif Containing 4)

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.

This post-translational modification triggered the rearrangement of the actin cytoskeleton in PC cells by altering the transcriptional levels of MYH9, thereby promoting PC malignancy. Overall, our findings demonstrate that neddylation of RNF187 enhances PC malignancy through the IQGAP1/MYH9 axis, suggesting a new therapeutic target for PC.

Beyond classical immune genes, recent GWAS have identified novel loci including SPATA16 (spermatogenesis associated 16), ABT1 (activator of basal transcription 1), IER3 (immediate early response 3), Adaptor Related Protein Complex 4 Subunit Beta 1 (AP4B1), Tripartite Motif Containing 45 (TRIM45), Patatin Like Phospholipase Domain Containing 1 (PNPLA1), and PRRC2A (proline-rich coiled-coil 2 A) that are implicated in transcriptional regulation, stress response, RNA processing, and intracellular transport, all of which may modulate viral replication and persistence. Understanding these genetic determinants provides new insights into host-virus interactions and offers opportunities for selective breeding strategies, biomarker development, and improved BLV control programs.

Importantly, we found that TRIM44 promotes K48-linked polyubiquitination of vimentin through its B-box domain, thereby targeting vimentin for proteasomal degradation. Collectively, our study establishes TRIM44 as a critical regulator of ccRCC progression through vimentin destabilization, highlighting its potential as both a prognostic biomarker and therapeutic target for ccRCC.

Moreover, indole-3-carbinol, interferon gamma-1b, and pretomanid (targeting IFNGR1) are potential keloid treatments...IFNGR1 was associated with the pathogenesis of keloids. Interferon gamma-1b targeting IFNGR1 might be a potential strategy for the treatment of keloids, and this discovery opened up a new direction for the treatment of keloids.

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.

Notably, TRIM44 conferred chemoresistance to doxorubicin in DB cells by increasing autophagic activity...The results of miRNA pull-down and luciferase reporter assay indicated that TRIM44 was a direct target of miR-665. In conclusion, TRIM44 promoted DLBCL progression by increasing autophagy-mediated chemoresistance, revealing the involvement of miR-665/TRIM44 axis.

GAPDH K251-Su enhanced glycolysis and glutamine reductive carboxylation to meet the demands for cell growth and to support survival in hypoxic and nutrient-depleted conditions, promoting tumor growth and metastasis. These findings indicate that tobacco smoking mediates metabolic reprogramming of cancer cells through succinylation of GAPDH to drive NSCLC progression.

NAT10 knockdown improved DDP sensitivity in NSCLC by inhibiting the TRIM44/PI3K/AKT pathway, which may have significant clinical implications for overcoming DDP resistance in NSCLC treatment.

TRIM46 overexpression also activated NF-κB signaling in PC cells. To sum up, ONECUT3 has been identified as a promising prognostic indicator in PC, and targeting this cancer-promoting pathway could offer an effective therapeutic approach to combat the PC progression.

TRIM44 exerts as an oncogenic factor to induce the oncogenesis of MM by stabilizing ZEB1.

Notably, pre-treatment with reparixin, a CXCR1/2 inhibitor, blocked OC-MQ-induced TRIM46 expression and cell invasion. These results suggest that CXCL8 derived from TAMs promotes human ovarian cancer cell invasion via the Wnt/β-catenin pathway by upregulating TRIM46.