MYH4 (Myosin Heavy Chain 4)

FLASH provides an efficient and robust tool for high-throughput skeletal muscle histology. By combining enzymatic and fluorescent co-labeling with machine learning-based image analysis, this method improves reproductibility, reduces experimental complexity, and minimizes user bias. FLASH is particularly well-suited for large-scale or longitudinal studies investigating muscle adaptation in health and disease.

Our data suggest that myonuclei fate occurs prior to overt muscle wasting when cachexia gene expression only modestly overlaps with differentiation factors, with a strong association after irreversible muscle wasting. These findings explain the challenge of effectively targeting skeletal muscle wasting in cancer cachexia requires addressing the changing cell population induced through non overlapping mechanisms.

Notably, Myh4 disruption accelerated mouse mammary tumorigenesis in a Trp53-deficient background. In conclusion, our results suggest an unanticipated function of MYH4 in p53-mediated tumor suppression that can explain their combined loss in breast cancer.

Additionally, molecular docking studies demonstrated strong binding interactions between key CRPC-related genes (ABCC4 and FOLH1) and potential therapeutic ligands, including flutamide and N-acetyl glucosamine (NAG), highlighting their therapeutic potential in overcoming drug resistance. These findings provide novel insights into the molecular landscape of CRPC and support the development of precision-targeted therapies to improve patient outcomes.

All patients received concurrent chemoradiotherapy (CCRT) utilizing intensity-modulated radiation therapy alongside concurrent chemotherapy with a cisplatin-based regimen...We concluded that specific mutations correlated to the pathological complete response in ESCC receiving neoadjuvant chemoradiation can be identified through the utilization of 35-gene expression profiles. Further investigation into the pathophysiological roles of MUC17 and MUC4 mutations in ESCC is warranted.

Immune infiltration and drug susceptibility results provide important clues for finding new personalized treatment options for COAD. These findings may facilitate personalized cancer treatment.

High expression of MYH1, MYH4, FGG, DEPP1, and ZBTB16 was associated with shorter overall survival of patients with cervical cancer; high expression of SULT1E1, RAB3C, CXCR3, and PROX2 was associated with longer overall survival of patients with cervical cancer. In conclusion, the transdermal peptide PKU12 is potentially a good candidate for a siRNA delivery vehicle for the treatment of cervical cancer.

These data show that pancreatic tumour organoid-derived factors alter the kinetics of myogenesis, which may eventually contribute to impaired muscle mass maintenance in cancer cachexia.

These results show that in C2C12 cultures, TMVs are able to affect both differentiation and the mitochondrial system. Such effects could be related to TMV-contained miRs.

These results add data to the interesting question about the link between physical activity, muscle physiology and protection against colorectal cancer. The two phenomena have in common the cytoskeleton remodelling, due to the TPM4 activity, that is involved in stress fibres formation.