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Mechanisms of lung squamous cell carcinoma (LSCC) development are poorly understood. Here, we report that JNK1/2 activities attenuate  Lkb1 -deficiency-driven LSCC initiation and progression through repressing ΔNp63 signaling. In vivo  Lkb1  ablation alone is sufficient to induce LSCC development by reducing MKK7 levels and JNK1/2 activities, independent of the AMPKα and mTOR pathways. JNK1/2 activities is positively regulated by MKK7 during LSCC development. Pharmaceutically elevated JNK1/2 activities abates  Lkb1  dependent LSCC formation while compound mutations of  Jnk1/2  and  Lkb1  further accelerate LSCC progression. JNK1/2 is inactivated in a substantial proportion of human LSCC and JNK1/2 activities positively correlates with survival rates of lung, cervical and head and neck squamous cell carcinoma patients. These findings not only determine a suppressive role of the stress response regulators JNK1/2 on LSCC development by acting downstream of the key LSCC suppresser  Lkb1 , but also demonstrate activating JNK1/2 activities as a therapeutic approach against LSCC.

JNK1/2 represses Lkb1-deficiency-induced lung squamous cell carcinoma progression