CHRNA7 (Cholinergic Receptor Nicotinic Alpha 7 Subunit)

In a mouse xenograft model, acetylcholine administration accelerated tumor growth in animals bearing control pancreatic cancer cells but not in those implanted with nAChR-α7-knockdown cells. Collectively, our findings reveal a novel mechanism of acetylcholine-induced enhancement of HIF-1α expression involving PDPK1/YAP signaling and highlight the utility of HIF-1α as a therapeutic target in acetylcholine-potentiated pancreatic cancer.

Perturbagen analysis nominated signature-reversing compounds across sexes, including histone deacetylase inhibitors, Aurora kinase inhibitors, microtubule-targeting agents such as vindesine, and multi-kinase inhibitors targeting VEGFR, PDGFR, FLT3, PI3K, and MTOR. Glioma grade comparisons reveal a shared neuronal-synaptic program accompanied by sex-specific transcriptional remodeling. These findings support sex-aware therapeutic strategies that pair modulation of neuron-glioma coupling with chromatin- or receptor tyrosine kinase/angiogenic-targeted agents, and they nominate biomarkers such as GLI1, MYOD1, GCGR, PRLHR, and HIST1H2BH for near-term validation.

Differential expression of CHRNA3, CHRNA5, and CHRNA7 indicates different EMT states in OSCC/HNC, influencing proliferation, differentiation, cell adhesion, immune reactions, and treatment efficacy, and warrants further experimental validation.

Data-mining (GLASS-database) showed that recurrent GBM in females with an elevated EGR1 and methylated MGMT promoter had a shorter survival. In summary, GBM with increased EGR1 expression, Ki67-labeling in EGR1high tumor and angiogenesis demonstrated a poor-response to bevacizumab, suggesting EGR1 could be useful in predicting response.

Patients with high expression of CHRNA7 have a relatively worse prognosis. Nicotine may upregulate PD-L1 expression in LUSC through the α7-nAChR/STAT3 pathway.

The antitumorigenic effects of AR-R17779 were linked to an adaptive immune response based on in vivo studies showing a survival benefit when AR-R17779 was administered as a combination therapy with anti-PD-L1, demonstrating that the effects of AR-R17779 were dependent on CD8 T cells, and in vitro studies showing AR-R17779 treatment of dendritic cells increased T cell activation. Together these findings supported the importance of CHRNA7 as a novel therapeutic target expressed on dendritic cells based on its role in potentiating the adaptive immune response in mouse models of breast cancer.

The therapeutic promise of naringenin was further supported by its considerable reduction in tumor weight and volume shown in animal trials. This study shows that naringenin may regulate signaling pathways by targeting a series of genes: IGFBP3, PGF, CA9, AKR1C3, KLK1, and CHRNA7, resulting in the inhibition of tumor cell proliferation and metastasis, alongside the promotion of apoptosis.

Our region-based approach identified 11 genomic regions that suggest association with glioma risk of which two regions, 16p13.3 and 1p36.21, warrant further investigation as genetic susceptibility regions for female and male risk respectively. Our analyses suggest that genetic susceptibility to glioma may differ by sex and highlights the possibility that synapse-related genes play a role in glioma susceptibility.

Sesamin can promote proliferation and inhibit apoptosis in human trophoblasts by downregulating EGFR and CASP3 expression and upregulating PTGS2 expression. Our findings play an important role and basis for further research into the molecular mechanism of SC treatment of RSA and drug development of TNFi.

We identified a total of 188 SFARI ASD genes (17%) carrying pathogenic variants in our cohort:122 and 66 genes in cases and controls, respectively. Cases included 111 high-confidence, strong candidate ASD genes that were enriched for nervous system development (p- 1e-05), axon guidance (2.6e-7), opening of presynaptic calcium channels (3.5e-05) and oligodendrocyte precursor cell markers (2.23e-05). 28 genes were common to both SCZ and BP subjects which were significantly enriched for genes CACNA1G, CACNA2D1, CHRNA7, CACNA1E, and CACNA1B involved in presynaptic voltage-gated calcium channel activity (5.26e-07).

None of the DNT negative compounds dysregulated any of the 9 DEGs in common for the DNT positive compounds. We suggest that SEMA5A or CHRNA7 should be further evaluated as biomarkers for DNT studies in vitro since they also are involved in neurodevelopmental adverse outcomes in humans.

Furthermore, we identified common genes that may be involved in the interaction between the MMR system and NTRK gene alterations in HAS. These results may have important implications for the development of targeted therapies for gastric cancer.