Skip to main content
. Author manuscript; available in PMC: 2023 Mar 7.
Published in final edited form as: Pharmacol Ther. 2022 Apr 29;239:108199. doi: 10.1016/j.pharmthera.2022.108199

Fig. 3.

Fig. 3.

Schematic showing how acetylcholine and its antagonist affect cell apoptosis, cell proliferation, and tumorigenesis. Ach binding to muscarinic acetylcholine receptor M1 (M1R) induces EGFR-mediated tumorigenesis via MMPs and enhances cell proliferation. Muscarinic acetylcholine receptor M3 (M3R) promotes tumorigenesis through the ERK1/2 and AKT pathways. M3R increases cell proliferation by activating MMP7, which induces the ERK1/2 and PI3K/AKT pathways regulated by the EGFR signal. 4-DAMP, an M3R antagonist, promotes cell apoptosis via caspase-3 and Bax in mitochondria by inhibiting the ERK and AKT pathways. Tuft cells and nerves release ACh, upregulating NGF expression, which promotes cancer cell proliferation in gastric epithelium. The figure was created with BioRender.com.