LKB1 Phosphorylation and Deactivation in Lung Cancer by NNAL, a Metabolite of Tobacco-Specific Carcinogen, in an Isomer-Dependent Manner

Investigators reported that NNAL, a major metabolite of a tobacco-specific carcinogen NNK, induced LKB1 phosphorylation and its loss of function via the β-AR/PKA signaling pathway in an isomer-dependent manner in human lung cancer cells.