Weng Chengyin, Chen Yong, Wu Yong, Liu Xia, Mao Haibo, Fang Xisheng, Li Baoxiu, Wang Lina, Guan Mingmei, Liu Guolong, Lu Lin, Yuan Yawei
Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People's Republic of China,
Department of Medical Oncology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou 510180, People's Republic of China,
Onco Targets Ther. 2019 Apr 8;12:2553-2561. doi: 10.2147/OTT.S196132. eCollection 2019.
The human ubiquitination factor E4B (UBE4B) gene is frequently amplified in some solid cancers. However, the role of UBE4B in nasopharyngeal carcinoma (NPC) has not yet been investigated.
Firstly, we analyzed the expression of UBE4B in NPC samples using real-time quantitative PCR and Western blot analysis. After knocking down UBE4B using small interfering RNA technology, the functions of UBE4B on cell proliferation, apoptosis, and cell cycle, as well as underlying mechanism, were investigated.
Compared with matched adjacent non-tumor tissues, both protein and mRNA levels of UBE4B were much higher in most NPC cancerous specimens. Deficiency of UBE4B could significantly inhibit tumor cell growth and induce cell apoptosis. Knocking down UBE4B could promote the expression of cleaved caspase3 and p53, and inhibition of caspase3 could prevent cell apoptosis induced by the deficiency of UBE4B.
These results indicate that expression of UBE4B was higher in most NPC tissues compared to adjacent non-tumoral tissues, and that knockdown of UBE4B inhibited the cell growth and induced apoptosis in NPC cells. This process was regulated by the activation of caspase3 and p53. Thus, UBE4B gene might act as a potential molecular target to develop novel strategy for NPC patients.
人泛素化因子E4B（UBE4B）基因在某些实体癌中常发生扩增。然而，UBE4B在鼻咽癌（NPC）中的作用尚未得到研究。
首先，我们使用实时定量PCR和蛋白质印迹分析来检测NPC样本中UBE4B的表达。利用小干扰RNA技术敲低UBE4B后，研究UBE4B对细胞增殖、凋亡和细胞周期的影响及其潜在机制。
与配对的相邻非肿瘤组织相比，大多数NPC癌组织样本中UBE4B的蛋白质和mRNA水平均高得多。UBE4B的缺失可显著抑制肿瘤细胞生长并诱导细胞凋亡。敲低UBE4B可促进裂解的caspase3和p53的表达，抑制caspase3可阻止因UBE4B缺失诱导的细胞凋亡。
这些结果表明，与相邻非肿瘤组织相比，大多数NPC组织中UBE4B的表达更高，敲低UBE4B可抑制NPC细胞的生长并诱导其凋亡。这一过程受caspase3和p53激活的调控。因此，UBE4B基因可能作为一个潜在的分子靶点，为NPC患者开发新的治疗策略。
