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UC2288通过抑制EGFR/ERK通路诱导鼻咽癌细胞凋亡。

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

作者信息

Liang Renba, Zhu Xiaodong

机构信息

Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, P.R. China.

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, P.R. China.

出版信息

J Cancer. 2021 Jan 1;12(4):988-995. doi: 10.7150/jca.48282. eCollection 2021.

DOI:10.7150/jca.48282
PMID:33442398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7797659/
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.

摘要

放射疗法和化学疗法是鼻咽癌（NPC）患者的标准治疗方法。这些治疗会引起一些严重的毒性反应，约30%的患者在治疗后会出现复发和转移。UC2288在结构上与多激酶抑制剂索拉非尼相似。然而，关于UC2288对肿瘤作用的研究很少。在此，UC2288以剂量和时间依赖性方式抑制NPC细胞的增殖并诱导其凋亡。通过蛋白质免疫印迹法和免疫荧光测定，我们发现UC2288促进了DNA损伤。此外，UC2288降低了表皮生长因子受体（EGFR）和细胞外信号调节激酶（ERK）的磷酸化水平。而且，用表皮生长因子（EGF）预处理可部分挽救被UC2288抑制的细胞活力。总之，UC2288通过抑制EGFR/ERK通路抑制了NPC的生长，它可能是一种有前景的鼻咽癌治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/6a817bdf2a4b/jcav12p0988g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/b6e0e1e631e4/jcav12p0988g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/3e8be610b448/jcav12p0988g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/ab8d2bc6e664/jcav12p0988g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/35fc63e4792a/jcav12p0988g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/6a817bdf2a4b/jcav12p0988g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/b6e0e1e631e4/jcav12p0988g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/3e8be610b448/jcav12p0988g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/ab8d2bc6e664/jcav12p0988g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/35fc63e4792a/jcav12p0988g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c95/7797659/6a817bdf2a4b/jcav12p0988g005.jpg

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