Role of the JNK Pathway in Bladder Cancer

Abstract

Eun Hye Lee,1,* Hyun Tae Kim,2,* So Young Chun,3 Jae-Wook Chung,2 Seock Hwan Choi,2 Jun Nyung Lee,2 Bum Soo Kim,2 Eun Sang Yoo,2 Tae Gyun Kwon,2 Tae-Hwan Kim,2 Yun-Sok Ha2 1Joint Institution of Regenerative Medicine, Kyungpook National University, Daegu, Korea; 2Department of Urology, School of Medicine, Kyungpook National University, Daegu, Korea; 3BioMedical Research Institute, Kyungpook National University Hospital, Daegu, Korea*These authors contributed equally to this workCorrespondence: Tae-Hwan Kim; Yun-Sok Ha, Department of Urology, School of Medicine, Kyungpook National University, Daegu, Korea, Email [email protected]; [email protected]: Bladder cancer, one of the most frequently diagnosed cancers worldwide, is associated with high morbidity and mortality and a poor prognosis. The bladder cancer types include 1) non-muscle invasive bladder cancer (NMIBC) and 2) muscle invasive bladder cancer (MIBC). Metastases and chemoresistance in MIBC patients are the leading causes of the high death rate. c-Jun N-terminal kinase (JNK) is an important factor for the undifferentiated state of cancer cells. JNK belongs to the mitogen-activated protein kinases (MAPKs) family; it is activated by various extracellular stimuli, such as stress, radiation, and growth factors and mediates diverse cellular functions, such as apoptosis, autophagy, proliferation, invasion, and migration by mediating AKT (Ak strain transforming), ATG (Autophagy related), mTOR (Mammalian target of rapamycin), and caspases 3, 8, and 9. This review describes the JNK-related functions, mechanisms, and signaling in bladder cancer.Keywords: bladder cancer, JNK, proliferation, apoptosis, metastasis, chemoresistance, autophagy

Keywords

• bladder cancer
• jnk
• proliferation
• apoptosis
• metastasis
• chemoresistance
• autophagy.