TRIB3 (Tribbles Pseudokinase 3)

Knockdown of CDK6 or treatment with the CDK4/6 inhibitor Palbociclib diminished tumorsphere formation and expression of stemness markers (OCT4, NANOG, c-MYC) in both conventional and patient-derived EC cells...In EC specimens, ELF4, TRIB3, and CDK6 expression positively correlated, and Kaplan-Meier analysis indicated that high co-expression of these genes predicted the poorest overall survival. Collectively, our findings establish the ELF4/TRIB3/CDK6 axis as a critical regulator of EC progression and CSC maintenance, highlighting its potential as a therapeutic target for EC.

LR group had lower TIDE scores and lower IC50 values (Alpelisib, Ibrutinib, Sapitinib, and Savolitinib). Patients in LR group had potential advantages in survival, immune response, and drug sensitivity. In summary, the results offered new insights into prognosis prediction, immunotherapy, and personalized treatment of LUSC.

Our findings reveal that LFQSNY laser inhibits the melanogenesis of melanocytes and enhances the effect of anti-inflammation for improves pigment-clearance in melasma via a non-thermal photobiomodulation. The insights provide a mechanistic rationale for enhancing clinical efficacy of LFQSNY laser-therapy in melasma.

All our findings provide hypotheses for PFOS/PFOA-induced tumorigenesis; however, experimental studies are required to establish translational relevance. All the R codes developed in this study are publicly available.

TRIB3 could promote the progression of EC through interacting with E2F1 and enhancing PKM2-mediated tumor glycolysis.

We detail two distinct solid-tumor circuits: (i) inducible TRIB3 overload in KRAS- or EGFR-mutant lung adenocarcinoma that triggers lethal paraptosis when mTOR is inhibited by everolimus plus ginsenoside Rh2; (ii) VHL-controlled UBE3B abundance in breast carcinoma, where loss of VHL renders tumors dependent on TRIB3 shielding for sustained MYC signaling...Remaining translational challenges-efficient intracellular delivery, biomarker-guided patient selection, and off-target surveillance-are increasingly tractable thanks to advances in peptide formulation, AI-accelerated screening, and established regulatory paths for targeted degraders. Collectively, current evidence positions the TRIB3-MYC interface as a druggable Achilles' heel and a realistic gateway to long-sought direct MYC blockade in the clinic.

Pharmacological inhibition of MCU with berberine suppressed GSC growth and extended survival in mouse GBM models. These findings establish MCU as a critical link between mitochondrial metabolism and epigenetic regulation, highlighting its potential as a therapeutic target for glioblastoma.

Our findings suggest that METTL14 suppressed TRIB3 expression via an m6A-YTHDF2-dependent manner, thus inducing ferroptosis to inhibit the malignant progression of CRC. TRIB3 is potentially exploited as a molecular target for CRC treatment based on ferroptosis.

TRIB3 overexpression can enhance Cx43 expression in human GCs by inhibiting the Wnt/β-catenin pathway, thereby reducing oocyte maturation rate. These findings could be used to improve the quality of female oocytes and enhance infertility therapy in the clinic.