MAPK14 (Mitogen-Activated Protein Kinase 14)

Importantly, YHD enhanced the sensitivity of OS cells to cisplatin, demonstrating a synergistic inhibitory effect in vitro and in an orthotopic OS mouse model. These findings suggest that YHD exerts its anti-osteosarcoma effects via reactive oxygen species-mediated mitochondrial disruption and pathway modulation, and may serve as a promising adjuvant to conventional chemotherapy.

Mechanistically, EHDPP binds to EGFR and inhibits its ubiquitination-mediated degradation, thereby stabilizing EGFR protein and partly activating the downstream PI3K-AKT signaling pathway, which ultimately promotes lung cancer cell proliferation and migration. This study is the first to elucidate the molecular mechanism underlying the pro-carcinogenic effects of EHDPP at the interaction level, providing potential molecular marker clues and mechanistic basis for EHDPP-related environmental risk assessment.

Collectively, our results provide a theoretical framework for understanding the complex mechanisms mediating ATBC-induced myocardial damage. They also offer crucial insights for developing preventive and therapeutic strategies targeting cardiac disorders potentially arising from exposure to ATBC-containing plastic products or environmental ATBC contamination.

Molecular docking suggested that DINP can potentially interact with key targets, especially MAPK14 and FAAH. Our findings suggest that DINP may promote GC development through interactions with core targets like MAPK14, highlighting its potential role as an environmental risk factor and a candidate biomarker.

This study offers a theoretical basis for the clinical use of Inula helenium in liver cancer treatment and encourages further investigation.

This study enhances our understanding of ARID1A regulatory mechanisms, highlighting its phosphorylation as a key driver of breast cancer biology. Future research should validate these kinase-substrate interactions and explore their transcriptional and chromatin-level impacts to develop precision therapies for ARID1A-dysregulated cancers.

Using high-throughput screening, we established that combining p38 inhibitors with the BRAF inhibitor dabrafenib showed strong synergy in vitro, including in cells resistant to dabrafenib and trametinib that had acquired a secondary TP53 mutation. Overall, our findings suggest an oncogenic link between the MAPK and p38/MAPK14 pathways and that combining p38 pathway inhibitors with dabrafenib-targeted therapy could improve treatment outcomes for aggressive thyroid cancers. However, more specific and effective p38 inhibitors are required to fully harness this potential.

This study identifies an SLC39A10-MAPK14-M2 macrophage regulatory axis that critically influences immune microenvironment remodeling and GC progression. Targeting this signaling axis may provide a viable therapeutic approach to alter the TME and suppress disease advancement.

An 18-month HFD successfully established a translational M. fascicularis model replicating key metabolic disorders (MASH, diabetes, cardiac hypertrophy). BAAT, CS/MDH1/H6PD, and SRC/MAPK14/EMD/ITGB1 were identified as mechanistic biomarkers for these conditions.

Consistently, qPCR and Western blot analyses of mouse brain tissue homogenates revealed that DAO expression was significantly downregulated, whereas PTGS1, MMP8, MAPK14, and BCHE were significantly upregulated, consistent with computational predictions. These findings provide a novel molecular framework for understanding the link between environmental pollutants and mental disorders, confirming the neurotoxic effects of bisphenol compounds.

For left-sided colon cancer, glucose-6-phosphate (G6P), ATP, ADP, glycerol, and palmitoyl-CoA were key metabolites forming the basis of the gene-metabolite network, along with genes including G6PD, PFKL, MAPK14, FLT1, CDK4, AURKA, MAP2K1, ERCC3, TP53, WEE1, and GPD2. These findings highlight distinct molecular profiles between right- and left-sided colon cancers, particularly in pathways related to angiogenesis, apoptosis, ferroptosis, and fatty acid metabolism, which may inform therapeutic strategies.

Future research should focus on combining multi-omics data with AI-driven approaches to improve biomarker discovery, optimize patient classification, and guide personalized treatments. Bridging the gap between molecular insights and clinical applications will enable precision medicine strategies, improving early diagnosis and therapeutic outcomes in axSpA.