SEMA7A (Semaphorin 7A)

Furthermore, CAF-derived SEMA7A engaged ITGB1 on GC cells and initiated ERK1/2-CEBPB signaling to transcriptionally upregulate GAL3ST1. Collectively, these findings reveal a role for GAL3ST1 in histone sulfation-mediated epigenetic regulation and elucidate the SEMA7A/GAL3ST1/H3Y99sulf axis as a crucial mediator of tumor-stromal crosstalk in GC metastasis.

Conversely, Kdm4a overexpression reversed the antitumor effects of Sema7a deficiency. Our findings establish the Sema7a-Kdm4a axis as a crucial mechanism shaping the immunosuppressive microenvironment in breast cancer and highlight its potential as a therapeutic target to enhance antitumor immunity.

We established a new prognostic model based on DAIs for predicting clinical outcomes and therapeutic response of patients with primary liver cancer.

Blockade of fatty acid oxidation may reverse the immunosuppressive phenotype of TAMs and the outcomes of NSCLC. Our findings provide experimental evidence that SEMA7A may act as a regulatory factor for macrophage lipid metabolism, which influences the polarization status of TAMs.

In vitro experiments revealed that most of the seven ERGs were overexpressed in LUAD cells, and that SEMA7A knockdown could suppress LUAD cell proliferation, migration and invasion. Our results provided novel insights for the prognosis prediction and personalized treatment of LUAD.

This study combines proteomics and bioinformatics to predict and explore potential immune targets for synergistic chemotherapy against neuroblastoma, providing a new direction for clinical treatment that warrant further validation.

Our findings demonstrate a complex stiffness/SEMA7A/integrin β1/AKT/p300 cascade mediating reciprocal interactions between GFs and GBC cells, offering a potential therapeutic target for patients with GBC.

We further show SEMA7A's pro-metastatic phenotype and abrogate it via a function-blocking antibody. Collectively, these results highlight the impact aging has on the mammary gland and the risk for breast cancer tumorigenesis.

These findings suggest SEMA7A as a candidate for further research in ACC biology and a candidate for cancer therapy, as well as a potential prognosis biomarker for ACC patients.

This study reveals the functional heterogeneity of mast cell subpopulations in the CRC tumor microenvironment and their differential roles in tumor progression. Identification of mast cell subpopulation-specific marker genes provides new molecular targets for clinical diagnosis, prognostic prediction, and personalized immunotherapy in CRC.

Furthermore, we discuss the potential clinical applications of SEMA7A modulation, focusing on its significance as a potential biomarker and target. Collectively, by highlighting the structural intricacies and interactional dynamics of SEMA7A, this review provides substantial evidence supporting SEMA7A as a viable therapeutic target and offers strategic insights for drug development targeting SEMA7A.