JNK pathway inhibition enhances chemotherapeutic sensitivity to Adriamycin in nasopharyngeal carcinoma cells

Liu,Yong; Feng,Jing; Zhao,Ming; Wu,Jingbo; Fan,Juan; Wen,Qinglian; Xu,Jinhui; Zhang,Jianwen; Fu,Shaozhi; Wang,Biqiong; Lu,Yun; Xiong,Kang; Xiang,Li; Zhang,Yanling; Yang,Linglin

doi:10.3892/ol.2017.6349

JNK pathway inhibition enhances chemotherapeutic sensitivity to Adriamycin in nasopharyngeal carcinoma cells

Authors:
- Yong Liu
- Jing Feng
- Ming Zhao
- Jingbo Wu
- Juan Fan
- Qinglian Wen
- Jinhui Xu
- Jianwen Zhang
- Shaozhi Fu
- Biqiong Wang
- Yun Lu
- Kang Xiong
- Li Xiang
- Yanling Zhang
- Linglin Yang
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Affiliations: Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China
Published online on: June 8, 2017 https://doi.org/10.3892/ol.2017.6349
Pages: 1790-1794

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Abstract

The role of c-Jun N-terminal kinases (JNKs) in the pathogenesis of cancer is well‑known due to their involvement in carcinogenesis. Although previous studies have discussed different functions of JNKs depending on cell type, the present study aimed to investigate the function of JNKs in nasopharyngeal carcinoma (NPC) cells, as well as their involvement in chemotherapy sensitivity to Adriamycin. The present results showed that Adriamycin administration reduced cell viability and led to elevated expressions of c‑Jun, phosphorylated JNK and phosphorylated c‑Jun, indicating an activated JNK pathway. Notably, JNK inhibition by SP600125 also reduced cell growth. Thus, Adriamycin treatment combined with SP600125 was more effective on cell growth inhibition than each agent alone. The apoptosis analysis confirmed the reduction in cell growth. Therefore, these data provide evidence that the JNK pathway activity is negatively associated with cell viability, and its decline could sensitize NPC cells to Adriamycin.

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