TRIB3 (Tribbles Pseudokinase 3)

To address this, an antioxidant-enriched hydrogel (PG-gel) was developed from N-acetylcysteine-modified gelatin and poly (ethylene glycol) succinimidyl succinate, loaded with conditioned medium from umbilical cord mesenchymal stem cells (CM-UCMSCs)...Transcriptomic analysis revealed downregulation of apoptosis-related genes (e.g., Ddit3, Trib3 and Hmox1) and upregulation of mitochondrial metabolism genes (e.g., Mt-atp8, Mt-nd1 and Mt-cyb). In conclusion, the PG + CM-UCMSCs system provided comprehensive protection to cryopreserved ovarian tissue by mitigating oxidative stress, fibrosis, and apoptosis, likely through regulation of apoptotic signaling and enhancement of mitochondrial energy metabolism, thereby offering a promising strategy to improve OTCT outcomes.

ISO inhibits NSCLC through direct targeting and downregulation of TRIB3, thereby inducing oxidative stress and suppressing the antioxidant Nrf2 pathway. Furthermore, ISO regulates the tumor microenvironment by promoting M1 macrophage polarization. These findings may contribute to improved prognosis for NSCLC patients and provide insights into the mechanism of ISO as an antitumor drug, thereby supporting its potential for clinical translation.

Moreover, TRIB3, via its involvement in ferroptosis, may serve as a potential therapeutic target for both HPV-positive and HPV-negative HNSCC. Thus, the present study has provided a starting point for further investigation into the therapeutic potential of targeting TRIB3.

This analysis identified 8 EDCs potentially involved in ccRCC: Diethylnitrosamine, Diethylstilbestrol, Resveratrol, 4,4'-diaminodiphenylmethane, Trichloroethylene, Arsenic, Lead, and 2,3,5-(triglutathion-S-yl)hydroquinone...Furthermore, cell-cell communication analysis revealed distinct signaling patterns among EDC-associated subpopulations, offering new insights into how EDCs may modulate gene expression and contribute to ccRCC progression. This study provides a foundation for future investigations into EDC-driven tumor biology and may guide the development of targeted therapies and preventative strategies against ccRCC.

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.