MAPK10 (Mitogen-Activated Protein Kinase 10)

We demonstrate that the endonuclease SND1 is SUMOylated at K513 in response to stresses such as oxidative stress and Cisplatin...Together, our findings reveal a novel oncogenic axis in which stress-induced SUMOylation of SND1 links tumor microenvironment stress to miRNA degradation. This SUMO1-SND1/miR-chr5_25226/MAPK10 pathway identifies the targeting of SND1 SUMOylation as a potential therapeutic strategy to modulate oncogenic miRNA decay and enhance chemosensitivity.

We validated MAPK10 promoter hypermethylation and CCL18 overexpression as prognostic biomarkers in ABC DLBCL. These findings, derived from integrative transcriptomic and immunogenomic profiling, provide clinically relevant insights into disease biology and support biomarker-guided strategies for precision treatment in aggressive B-cell lymphomas.

Furthermore, high MAPK10 expression was associated with a favorable prognosis in NSCLC patients, as evidenced by a hazard ratio (HR) of 0.42 (95 % confidence interval: 0.28-0.63). Collectively, these findings establish the MAPK10/KRT16/RNF213 axis as a promising therapeutic target and prognostic biomarker for NSCLC metastasis, providing new directions for the development of personalized treatment strategies.

The injection of hydrogen-rich water into the Zusanli (ST36) acupoint effectively inhibited the hyperplasia of 4T1 BC cells and enhanced their apoptosis, potentially exerting a therapeutic effect through multiple pathways and targeting various sites.

The EA fraction of A. argyi exerts potent anti-OvC activity by suppressing proliferation and migration, and by inducing apoptosis via JUN/MAPK10 signaling.

Our integrated approach underscores the value of MAPK family members as both biomarkers and therapeutic targets in LIHC and LUAD. This study contributes important insights into MAPK-related oncogenic processes and supports the development of targeted therapies under the framework of precision oncology.

Eight compounds (IIIa, b, c, d, f, g, h, and k) demonstrated superior antiproliferative activity compared to cisplatin, with potency ranging from 1.03- to 3.35-fold higher against the HepG2 cell line...Molecular docking simulations explained their significant CDK4 inhibition by demonstrating favorable binding interactions within the CDK4 active site. Finally, compounds IIId and IIIk induced cell cycle arrest in the G₀-G₁ phase in HepG2 cancer cells and promoted apoptosis and necrosis at levels 7.18- and 5.36-fold higher than control, respectively.

Notably, 879 multi-omic signatures include chimeric antigen targets currently under clinical evaluation, underscoring the translational relevance of our findings for precision oncology and immunotherapy. This integrative resource is publicly available via CancerRCDShiny (https://cancerrcdshiny.shinyapps.io/cancerrcdshiny/), supporting future efforts in biomarker discovery and therapeutic target development across diverse cancer types.

Overexpression of miR-222b-5p suppressed MAPK10 expression, thereby inhibiting apoptosis, enhancing cell viability, and accelerating cell cycle progression. These findings suggest that miR-222b-5p plays a vital role in REV infection-induced tumorigenesis.

This bioinformatics study delineates key matrisome-associated genes and pathways in HBV-related cirrhosis, offering novel insights into potential biomarkers and therapeutic targets. Further validation in larger cohorts is warranted to confirm clinical relevance.

HACD3 promotes the malignant progression of NSCLC by interacting with MKK7 and MAPK10 to suppress MAPK signaling, independent of its canonical dehydratase activity. The identification of a critical pro-oncogenic domain (aa231-259) suggests that targeting HACD3, potentially via this region, represents a novel therapeutic strategy for NSCLC.

The DNAm episignatures of MAPK10, PLCG1, PLCβ3 and PIK3R2 have a significant influence on radon-induced lung cancer. This brings a new perspective to understanding the pathways involved in radon-induced lung cancer and offers potential targets for developing blood-based biomarkers and epigenetic therapeutics.