CHRNB2, encoding the β2 subunit of the α4β2 nicotine acetylcholine receptor, is crucial in controlling neurotransmitter release. It is involved in various physiological and pathologic processes, with its associated pathways including the β -catenin, PI3K -AKT, and JAK -STAT pathways [1,2]. Genetic models, such as gene knockout in mice, can be valuable for studying its functions.

Knockdown of CHRNB2 in pancreatic cancer cells acetylcholine-independently increases cell migration and invasion, while overexpression decreases these abilities. This occurs through the inhibition of the β -catenin pathway, suggesting CHRNB2 negatively relates to lymph node metastasis in pancreatic cancer [1]. In gastric cancer, knockdown of CHRNB2 attenuates cell proliferation, and knockout significantly influences cell survival and metastasis-related functions. Anti-CHRNB2 monoclonal antibodies can inhibit gastric cancer cell growth in vitro and in vivo, as CHRNB2 interferes with the PI3K -AKT and JAK -STAT pathways [2]. In rats, nicotine vapor exposure reduces CHRNB2 expression, leading to increased risky choice [3].

In conclusion, CHRNB2 plays a significant role in multiple biological processes related to cancer metastasis and cognitive decision-making. Gene knockout or knockdown studies in models like pancreatic and gastric cancer cells, as well as in rats, have revealed its role in inhibiting cancer cell migration, invasion, and proliferation, and its impact on cognitive functions. This contributes to our understanding of related disease mechanisms, potentially providing new directions for treatment in cancer and nicotine-related disorders.