MYC (V-myc avian myelocytomatosis viral oncogene homolog)

This study identifies HSG as a critical tumor suppressor in malignant meningioma that restrains tumor aggressiveness by dampening the Wnt/β-catenin cascade. These novel findings highlight the HSG-Wnt/β-catenin axis as a promising therapeutic target, offering new translational strategies for the management of this highly aggressive intracranial tumor.

In conclusion, Hi-C sequencing detects gene rearrangements crucial for diagnosis in an unbiased and molecular manner and showed high sensitivity and specificity in our study. These advantages of Hi-C sequencing offer help to improve the workflow of clinical pathology laboratories, diagnostic precision, and treatment of large B-cell lymphoma.

This study comprehensively reveals YGJ's pharmacological properties against thyroid cancer, identifying its core targets and multi-pathway mechanisms.

Interestingly, unlike previous reports that emphasized protein-level regulation, our data reveal that, at this precise stage of differentiation, Trim32 regulates the stability of c-Myc at mRNA level. Attenuating c-Myc expression level is able to partially recover the myogenesis defects observed in the absence of Trim32, suggesting that the Trim32-c-Myc axis may represent an essential hub, although likely not the exclusive mechanism, in muscle regeneration within LGMDR8 pathogenesis.

Furthermore, the inhibitory effects of circ_0008777 knockdown on the cell migration and proliferation rates were rescued by c-Myc overexpression. In conclusion, circ_0008777 can promote HNSCC progression by upregulating c-Myc expression through both PC4- and miR-185-3p-related mechanisms, showing potential as a candidate therapeutic target in this cancer.

In addition, tumor cells exhibited a type II EBV latency pattern (LMP1+/EBNA2-) in 84.6% of cases, and LMP1 expression correlated with larger tumor size (p=0.021). Taken together, these findings support a role for EBV-driven activation of the cyclin D1 pathway and suggest that EBV-LMP1-CCND1 signaling may contribute to the pathogenesis of IFDCS.

XPO1 inhibition impairs HR and enhances radiosensitivity by disrupting the c-Myc-RAD51/CHEK1 axis. These findings support prospective evaluation of KPT-330-based radiosensitization in R/R ENKTL.

Mechanistically, treatment reduced p-EGFR, c-Myc, and HDAC1 expressions and activated apoptosis through caspase-2 independently of p53. These findings suggest that CCB-4 and its sugar complexes have promising anticancer effects against luminal A breast cancer cells by triggering caspase-2-mediated apoptosis and mitotic catastrophe.

The results suggested that GMPS may serve as a promising marker for the prognosis of HCC, and it may also be a potential therapeutic target for HCC. These findings may lay the theoretical foundation for the clinical application of GMPS.

Collectively, glycolytic reprogramming is not only a hallmark metabolic feature of LUAD but also a critical nexus linking immunosuppression, therapeutic resistance, and precision medicine. This review summarizes the molecular mechanisms, associated biomarkers, and targeted strategies of glycolytic reprogramming, aiming to provide insights for early screening, risk stratification, and metabolism-targeted therapies in LUAD..

When combined with CSF-1R inhibition and immune checkpoint blockade, the particles suppressed tumor growth, extended survival beyond 100 days, and achieved up to 50% complete remissions in Myc-overexpressing models. These findings position TLR-ferroptosis axis remodeling as a mechanistic blueprint for rational, particle-driven immunotherapies with broad translational potential in PCa and other immunologically refractory malignancies.

MIR22HG was notably positively correlated with β-catenin and C-myc, whereas it was negatively correlated with miR-10a-5p. This study highlights the clinical potential of serum MIR22HG and miR-10a-5p as novel diagnostic biomarkers and identifies MIR22HG and β-catenin as prognostic indicators, thereby paving the way for improved PC management.