Role of the JNK Pathway in Bladder Cancer.
Eun Hye LeeHyun Tae KimSo Young ChunJae Wook ChungSeock Hwan ChoiJun Nyung LeeBum Soo KimEun Sang YooTae Gyun KwonTae-Hwan KimYun Sok HaPublished in: OncoTargets and therapy (2022)
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.
Keyphrases
- muscle invasive bladder cancer
- signaling pathway
- cell death
- poor prognosis
- induced apoptosis
- endoplasmic reticulum stress
- pi k akt
- cell cycle arrest
- long non coding rna
- oxidative stress
- end stage renal disease
- chronic kidney disease
- newly diagnosed
- cell proliferation
- ejection fraction
- cell migration
- radiation therapy
- patient reported outcomes
- tyrosine kinase
- patient reported