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Nicotine stimulated OSCC malignancy through YAP-dependent BiP induction. Nicotine promoted malignant behaviors of OSCC, including EMT change, migration, and invasion, via inducing BiP expression. Mechanistically, nicotine increased BiP expression through α7-nAChR-Akt signaling and subsequent YAP dephosphorylation and nuclear translocation. Nuclear YAP together with TEAD increased HSPA5 promoter activity in OSCC cells after nicotine treatment.
