SEMA5A (semaphorin 5A)

These findings establish for the first time that SEMA5A is a novel player of melanoma aggressiveness and progression, modulating cancer cell viability and migration, focal adhesion signaling and lamellipodia formation in vitro and tumor growth in vivo.

The Sema5a-Plxna1 axis is an important mechanism for BHR-Ocys to regulate osteoclast differentiation. The study provides new insights into the role and mechanism of osteocytes in the regulation of bone homeostasis and identifies new targets for the prevention and treatment of osteoporosis.

Furthermore, ASCC3 may regulate tumor immunity by affecting T cell function. ASCC3 can serve as an independent prognostic factor for READ and can synergize with various immune-related genes to influence patient prognosis.

FZHWT demonstrates significant therapeutic potential in treating CAG by modulating inflammatory pathways and promoting mucosal repair. This study provides new insights into the treatment of CAG and supports the modernization of multi-component TCM formulas.

Notably, the EZH2 inhibitor Tazemetostat (EPZ-6438) exhibits greater sensitivity in cells with higher ZCCHC8 expression. Altogether, our findings demonstrate a novel mechanism that the NEXT complex regulates H3K27me3 levels by degrading nascent G4/U-Rich lncRNAs in cancer cells.

Furthermore, we demonstrated that transient over-expression of SEMA5A in H. pylori-infected cells inhibited CagA-mediated gain of mesenchymal phenotype. These results suggest that SEMA5A could be a key mediator of EMT and gastric carcinogenesis caused by CagA-positive H. pylori infection.

This study delved into the role of intestinal glycosylation changes, especially the O-GlcNAcylation, and forged a foundation for further research on the occurrence and development of UC. Overall, understanding the role of O-GlcNAcylation in UC could have significant implications for diagnosis and treatment, offering valuable insights into the disease's progression.

Our observation provided the first evidence of SEMA3F as a regulator of sensitivity to CDK4/6 inhibitors in breast cancer. The detailed mechanisms of resistance deserve further functional studies to develop the better strategy to overcome resistance in CDK4/6 inhibitors.

ARGs BMP6 and DLC1, associated with SEMA5A, were identified, and their prognostic significance in GC was demonstrated. Additionally, their regulatory mechanisms were further elucidated through immune infiltration analysis and molecular network construction, providing a theoretical foundation for future research on the molecular mechanisms in patients with GC.

We have identified core genes associated with non-small cell resistance to entrectinib, including CHI3L2, ZEB2, and S100A12. ZEB2 is a core gene associated with acquired resistance to entetinib in NSCLC.

The CCRGPI is reliable for predicting the prognosis and immunotherapy response of HSNCC patients and may be useful for guiding the individualized treatment of HNSCC patients.

Furthermore, the disease-free survival rate was increased in the groups with low expression of TP53I11, SH2D5, and SEMA5A. JQ-1 may act downstream of BRD4 and suppress ocular melanoma growth by inducing G1 cell cycle arrest.