CHRM3 (Cholinergic Receptor Muscarinic 3)

Molecular docking demonstrated the presence of affinity between target hub proteins and active compounds. This study revealed that SWT might exert its therapeutic effects on ESCC through multi-targets and multi-mechanisms.

Taken together, this study leverages LLM-guided discovery to delineate a novel ALKBH5/CHRM3/ZNF281 regulatory axis controlling ferroptotic susceptibility in PCa. Importantly, a synergistic therapeutic strategy was identified by combining RSL3 with AZD5363, providing novel therapeutic targets and directions for PCa treatment.

Finally, as we previously reported on the relevance of thymic stromal lymphopoietin (TSLP) in GBM pathophysiology, here, we found that TSLP upregulated CHRM3 expression. Our findings highlight the importance of the cholinergic system in the tumor microenvironment, where it may act directly on tumor cells or influence neutrophil physiology, thereby modulating tumor progression.

This article discusses the probable mechanism of action of semen strychni in the treatment of glioma, which can serve as a theoretical basis and evidence for subsequent experimental investigations.

These findings enhance our understanding of the molecular mechanisms by which BPA induces ccRCC and highlight potential targets for therapeutic intervention, particularly in endocrine and immune-related pathways. This underscores the need for collaborative efforts to mitigate the impact of environmental toxins like BPA on public health.

Collectively, these data indicate that submicromolar DZN promotes proliferation and suppresses apoptosis of GC cells by perturbing neuronal signaling networks. Our findings provide novel evidence linking environmental OP exposure to dysregulated neurotransmitter pathways in gastric carcinogenesis and highlight neuronal signaling components as potential therapeutic or preventive targets.

This previously unknown PJA2-CHRM3 signaling axis provides further understanding of cholinergic innervation as well as identifies a new therapeutic vulnerability in DGC.

Therapeutically, the anticholinergic drug scopolamine attenuates glioma growth, whereas the acetylcholinesterase inhibitor donepezil exacerbates disease. These findings reveal the complexity of neuron-glioma connectivity, highlighting long-range neuromodulatory pathways as promising therapeutic targets in GBM.

In xenograft mice bearing A549 tumors, CHRM3 knockdown showed little inhibition on tumor growth, but AMP treatment inhibited the tumor growth. AMP treatment inhibits the proliferation, migration, and invasion of lung cancer via the CHRM3/PI3K/AKT and CHRM3/MAPK pathways, thus exerting antitumor activity.

Pharmacological or genetic blockade of M1/M3 receptors abolished cholinergic activity-driven DMG proliferation. Taken together, these findings demonstrate that midbrain cholinergic long-range projections promote activity-dependent DMG growth, mirroring a parallel proliferative effect on healthy OPCs.

Deep single-cell RNA sequencing of co-cultures compared to GBM monocultures further revealed shifts in tumor transcriptional profiles toward a more proliferative state, with contributions from both diffusible factors and direct contacts, the latter of which are dependent on cholesterol biosynthesis. Together, our findings support the role of cholinergic inputs in promoting GBM progression and highlight hiPSC-derived co-culture models as a useful platform for cancer neuroscience.

P=N/A, N=220, Beijing Friendship Hospital of Capital Medical University; Beijing Friendship Hospital of Capital Medical University