Back to Journals » OncoTargets and Therapy » Volume 11

RGS17 inhibits tumorigenesis and improves 5-fluorouracil sensitivity in nasopharyngeal carcinoma

Authors Yu Q, Zhang N, Jiang Y, Huang Y, Lian YY, Liu T, Li N, Guan G

Received 6 June 2018

Accepted for publication 18 September 2018

Published 2 November 2018 Volume 2018:11 Pages 7591—7600


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Prof. Dr. Takuya Aoki

Qianqian Yu,1 Niankai Zhang,1 Yan Jiang,1 Yichuan Huang,1 Yuan-Yuan Lian,1 Tingting Liu,1 Na Li,1 Ge Guan2

1Department of Otorhinolaryngology, Affiliated Hospital of Qingdao University, Qingdao, China; 2Department of Organ Transplantation, Affiliated Hospital of Qingdao University, Qingdao, China

Background: Nasopharyngeal carcinoma (NPC) is a poorly differentiated malignant tumor, and 5-fluorouracil (5-FU) is one of the most effective chemotherapeutic drugs used for the treatment of NPC. Abnormal expression of RGS17 had been shown to improve the sensitivity of many cancers to chemotherapy; however, the effects of RGS17 on NPC remain unclear.
Methods: We cultured NPC cell lines and altered the RGS17 expression with vector. Subsequently colony formation assays and CCK8 cell viability assay was used to test the proliferation of NPC cells, flow cytometry was used to determine the percentage of apoptotic cells, MMP kit and flow cytometry was used to measure the mitochondrial membrane potential, and a xenograft tumour model was attached to investigate the effects of RGS17 on the growth of NPC cells in vivo. Additionally, RT-PCR and western blot was induced to examine the expression of RGS17 and the mechanism.
Results: Here, we report for the first time that RGS17 is downregulated in NPC cell lines and that RGS17 overexpression significantly reduces cell proliferation, decreases the mitochondrial membrane potential, and induces cell apoptosis in NPC cells. In vivo, RGS17 also inhibits the tumorigenicity of NPC. In addition, RGS17 could significantly improve the sensitivity of NPC cells to 5-FU. Furthermore, investigation into the underlying mechanisms showed that RGS17 upregulated the levels of IRE1α, p53, and active caspase-3 and cleaved PARP.
Conclusion: These results indicate that RGS17 could play important roles in the proliferation, apoptosis, and chemotherapeutic sensitivity of NPC cells.

Keywords: nasopharyngeal carcinoma, RGS17, cell apoptosis, mitochondrial membrane potential, fluorouracil chemotherapy

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]