Table 1.

Function of JNK in Bladder Cancer

Category	JNK Function	Corresponding References
Tumorigenesis	Phosphorylate AP-1 proteins Involved in AKT1 binding to JIP1	[32–40]
Cell proliferation	Regulate cell death and cell survival through FAS and TNF Inhibit JNK-enhanced bladder cancer cell apoptosis Inhibit cell growth via p21WAF1 activation Activate caspase-9, −8, and −3 Mediate apoptosis by regulating TGF-β1	[2,41–49]
Metastasis	Increase miR-200c transcription Decrease migration by inhibiting SOD2-induced JNK activation	[50–61]
Chemoresistance	Increase chemosensitivity through p53	[39,61,75,76]
Autophagy	Induce Bcl-2/Beclin-1 complex breakdown Activate autophagic reaction Attenuate gemcitabine-induced JNK activation through HMGB1 knockdown	[1,24,61–70]
Metabolism and Immune escape	Regulate lipid metabolism through MEX3C Enhance immune response by suppressing PD-L1	[71–74]

Abbreviations: AP-1, Activator protein 1; AKT, Ak strain transforming; JIP1, JNK-interacting protein 1; FAS, Fas Cell Surface Death Receptor; TNF, Tumor necrosis factor; JNK, c-Jun N-terminal kinases; p21WAF1, cyclin-dependent kinase inhibitor 1; TGF-β1, Transforming growth factor beta 1; SOD, Superoxide dismutase; Bcl-2, B-cell lymphoma 2; HMGB1, High mobility group box 1 protein, also known as high-mobility group protein; MEX3C, Mex-3 RNA Binding Family Member C; PD-L1, Programmed death-ligand 1.