J Cancer 2021; 12(4):988-995. doi:10.7150/jca.48282 This issue

Research Paper

UC2288 induces cell apoptosis of nasopharyngeal carcinoma cells via inhibiting EGFR/ERK pathway

Renba Liang1,2, Xiaodong Zhu1,2,3✉

1. Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, P.R. China.
2. Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, P.R. China.
3. Key Laboratory of Early Prevention and Treatment for Regional High‐Incidence‐Tumor, Guangxi Medical University, Ministry of Education, Nanning, Guangxi, P.R. China.

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Citation:
Liang R, Zhu X. UC2288 induces cell apoptosis of nasopharyngeal carcinoma cells via inhibiting EGFR/ERK pathway. J Cancer 2021; 12(4):988-995. doi:10.7150/jca.48282. Available from https://www.jcancer.org/v12p0988.htm

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Abstract

Radiotherapy and chemotherapy are the standard care for patients with nasopharyngeal carcinoma (NPC). These treatments cause some severe toxicity and about 30% of patients develop recurrence and metastases after treatment. UC2288 is structurally similar to sorafenib, a multikinase inhibitor. However, studies about the effects of UC2288 on tumors are few. Here, UC2288 inhibited proliferation and induced apoptosis of NPC cells in a dose- and time-dependent manner. Using western blot and immunofluorescence assay, we found that UC2288 promoted DNA damage. In addition, UC2288 decreased the phosphorylation of EGFR and ERK. Moreover, pretreatment with EGF partially rescued cell viability suppressed by UC2288. In conclusion, UC2288 suppressed the growth of NPC via inhibiting EGFR/ERK pathway and it may be a promising therapeutic option for NPC.

Keywords: nasopharyngeal carcinoma, UC2288, proliferation, apoptosis, EGFR/ERK pathway