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Silencing UBE4B induces nasopharyngeal carcinoma apoptosis through the activation of caspase3 and p53

Authors Weng C, Chen Y, Wu Y, Liu X, Mao H, Fang X, Li B, Wang L, Guan M, Liu G, Lu L, Yuan Y

Received 27 November 2018

Accepted for publication 4 February 2019

Published 8 April 2019 Volume 2019:12 Pages 2553—2561

DOI https://doi.org/10.2147/OTT.S196132

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Justinn Cochran

Peer reviewer comments 2

Editor who approved publication: Dr Federico Perche


Chengyin Weng,1–3,* Yong Chen,1,* Yong Wu,2,3 Xia Liu,2,3 Haibo Mao,2,3 Xisheng Fang,2,3 Baoxiu Li,2,3 Lina Wang,2,3 Mingmei Guan,2,3 Guolong Liu,2,3 Lin Lu,2,3 Yawei Yuan1,4

1Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People’s Republic of China; 2Department of Medical Oncology, Guangzhou First People’s Hospital, School of Medicine, South China University of Technology, Guangzhou 510180, People’s Republic of China; 3Department of Medical Oncology, Guangzhou First People’s Hospital, Guangzhou Medical University, Guangzhou 510180, People’s Republic of China; 4Department of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, People’s Republic of China

*These authors contributed equally to this work

Aim: 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.
Methods: 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.
Results: 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.
Conclusion: 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.

Keywords: UBE4B, nasopharyngeal cancer, apoptosis, caspase3, p53


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