Plcb1, short for phospholipase C beta 1, is a member of the phospholipase family involved in phospholipid hydrolysis. It is associated with multiple pathways such as the PI3K/AKT signaling pathway and plays a role in regulating the abundance of PI(4,5)P2 in the plasma membrane. Genetic models, like gene-knockout mouse models, have been crucial in studying its functions in various biological processes and disease conditions [1,2].

In cholangiocarcinoma, Plcb1 promotes tumor development and growth, activates the PI3K/AKT signaling axis to induce epithelial-to-mesenchymal transition (EMT), and confers resistance to gemcitabine combined with cisplatin treatment [1]. In gastric cancer, it enhances cell migration and invasion by regulating actin cytoskeletal remodeling and EMT [2]. In gliomas, increased oxygen stimulation affects chemoresistance and phenotype shifting through regulating Plcb1, which is involved in the proteasomal degradation of β-catenin and activation of the Wnt signaling pathway [3]. Heterozygous deletion of Plcb1 in mice reduces cue-induced reinstatement of cocaine-seeking behavior, suggesting its potential as a therapeutic target for cocaine addiction [4].

In conclusion, Plcb1 is essential in processes like tumor cell progression and addiction-related behaviors. Studies using KO/CKO mouse models have revealed its role in cholangiocarcinoma, gastric cancer, gliomas, and cocaine addiction, providing insights into potential therapeutic strategies for these disease areas.