SEMA4D (Semaphorin 4D)

Our study suggests that by antagonizing miR-214, HNF1A-AS1 activates the SEMA4D/PLEXIN-B1/TIAM/RAC pathway, facilitating EOC growth and potentially promoting M2 macrophage polarization in the tumor microenvironment. HNF1A-AS1 represents a compelling therapeutic target for treating EOC.

In this study, we demonstrate that the IGF2BP3/Sema4D axis is a crucial regulator in AML development, driving cell proliferation and survival through post-transcriptional regulation of Sema4D by IGF2BP3 in an m6A-dependent manner. Our findings highlight the potential of targeting this axis as a therapeutic strategy for AML treatment.

These findings provide a foundation for future clinical studies and targeted interventions to enhance recovery from PFP. Future research should focus on human sample validation to enhance clinical translation.

Four RBPs associated with SCI were identified: Nkrf, Marcks, NDRG4, and Ryr2. These key RBPs may serve as potential targets for the treatment of patients with SCI.

We also identify a female-specific association with CRC risk for CCM2 expression and subsite-specific associations, including LAMC1 with rectal cancer risk. These findings offer valuable insights into CRC molecular mechanisms and support promising therapeutic avenues.

Sema7A is involved in glial scar formation and may influence serotonin channel remodeling, thereby affecting motor coordination. Given these findings, the local or systemic application of neuronal guidance proteins represents a promising avenue for spinal cord injury treatment.

This study provides a robust immune-related prognostic model for melanoma. It underscores the value of immune gene expression and T cell infiltration, particularly CD8+ T cells, in predicting patient outcomes. The model facilitates personalized treatment decisions and advances precision oncology approaches in melanoma. The integration of transcriptomic analysis with experimental validation confirms the tumor-promoting role of KIR2DL4 and enhances the translational value of the model in guiding precision immunotherapy.

This study was the first to identify that DE exposure promotes the development of DEN-induced liver tumors in mice, with the mechanism potentially involving the SEMA4D/PI3K/AKT pathway. These findings provide novel insights into the hepatotoxic effects of DE and highlight the need for further investigation into its carcinogenic potential.

TRGS was identified as an independent prognostic indicator for melanoma, offering novel insights into the role of Tregs in modulating the TME. This study highlights the potential clinical utility of TRGs in melanoma diagnostics and personalized immunotherapy, providing a robust foundation for future therapeutic strategies.

This study provides proof of a causal relationship between genetically predicted 44 proteins associated with OC risk, which could serve as promising drug targets for OC.

Given the many physiological parallels between glial activation and inflammatory processes in HD and AD, prior results from the SIGNAL-HD trial suggest that preventing astrocyte activation and reducing brain inflammation with pepinemab treatment could be an attractive alternative or complement to anti-Aβ antibodies.

Herein, we designed a connexin blocker-carbenoxolone (CBX)-loaded biomimetic liposomal system with artificial liposomes fused with brain metastatic cell and reactive astrocyte membranes (LAsomes) to block gap junctions and attenuate chemoresistance...Consequently, LAsomes effectively inhibited material transfer and Ca2+ flow from metastatic cells to astrocytes via gap junctions, thereby markedly increasing the sensitivity of metastatic tumor cells to chemotherapy. These results reveal that closing the gap junctions may be a promising therapeutic strategy for intractable brain metastasis.