TRIB1 (Tribbles Pseudokinase 1)

Overexpression of miR-100-5p inhibits proliferation and induces apoptosis of HL-60 cells by downregulating TRIB1.

Our findings reveal that specific MASLD/MASH-associated genetic variants influence FIB-4 scores and are linked to cardiovascular and mortality outcomes in an elderly population. These results suggest that liver fibrosis may reflect not only hepatic injury, but also broader systemic vulnerability driven by genetic predisposition. Incorporating genetic risk profiles may improve stratification for both liver and cardiometabolic disease.

These findings suggest that these genes may serve as potential therapeutic targets for the prevention and treatment of comorbidities in patients with PCOS and MetS. The identified hub genes play significant roles in the development of PCOS and MetS, underscoring the need for further research on these genes. This study offers insights into molecular interactions and potential biomarkers for early diagnosis and therapeutic targets for these syndromes. Future studies should aim to validate these findings in larger cohorts to enhance their clinical applicability.

This deletion likely caused TRIB1 haploinsufficiency, reducing control over dysplastic clones and driving progression to MDS with increased blasts 2 (MDS-IB2) over three years. This first report of TRIB1 copy number loss in myeloid disorders highlights the value of SNP-array with patient-matched controls in distinguishing somatic variants, expanding MDS's genetic profile and underscoring TRIB1's context-dependent roles in oncogenesis.

Additionally, Prdm12 ablation remodeled the chromatin accessibility landscape, with H3K9me3 deposition at loci regulating T cell differentiation (Trib1 and Sgk1) and exhaustion (Rgs1 and Nr4a2). These results together reveal a negative regulatory mechanism for CD8+ T cells and advance our understanding of cancer immunotherapy by linking neurobiological signaling to immune regulation.

In addition, TRIB1 was preliminarily identified as the target for tRF ArgCCG involved in colon cancer progression. In conclusion, our study offers a novel perspective on the molecular mechanism of methyltransferase NSUN2 regulating the selective expression of tRFs in colon cancer under hypoxic conditions.

TRIB1 facilitated the proliferation and migration of OC cells by enhancing EMT progression.

Additionally, FAM83 homolog and TRIB1 unexpectedly harbored copy number amplifications. In conclusion, this study elucidated novel prognostic indicators for NSCLC that may serve as targets to overcome therapy resistance toward improved patient outcomes.

Chromatin accessibility analysis of the PBMCs from patients with early-stage breast cancer underscores its potential as a significant avenue for biomarker discovery in breast cancer diagnostics and treatment. By screening the transcription factors and DEGs related to breast cancer, this study provides a comprehensive theoretical foundation that is expected to guide future clinical applications and therapeutic developments.

COP1 downregulation also inhibits the proliferation of human AML cells in a TRIB1-dependent manner. Taken together, our results provide new insights into the role of Trib1/Cop1 machinery in the C/EBPα p42-dependent leukemogenic activity, and a novel idea to develop new therapeutics.

All these effects make TRIB1 a potential drug target. However, the lack of a catalytic domain renders TRIB1 "undruggable", but knowledge about its structure, conformational changes during substrate binding, and substrate binding sites provides an opportunity to design small-molecule inhibitors against specific TRIB1 interactions.

These effects were not mediated by the MAPK pathway. Our results suggest a tumor-suppressive function of TRIB2 in GC with a CIN phenotype.