Article Text

Download PDFPDF
UBR5 inhibits the radiosensitivity of non-small cell lung cancer cells via the activation of the PI3K/AKT pathway
  1. Yong-Fei Gu,
  2. Xing-Ping Ge
  1. Radiotherapy Department, Second Ward, Yantai Yantai Shan Hospital, Yantai, Shandong, China
  1. Correspondence to Dr Xing-Ping Ge, Radiotherapy Department, Second Ward, Yantai Yantai Shan Hospital, Yantai 264000, Shandong, China; Xinpingge6653{at}126-web.net

Abstract

Ubiquitin protein ligase E3 component n-recognin 5 (UBR5) has been identified as an oncogene in diverse cancers; however, whether its expression was associated with radiosensitivities of non-small cell lung cancer (NSCLC) cells remains unclear. Expression levels of UBR5 in NSCLC tissues and cell lines were examined by immunohistochemical staining and western blotting. Colony formation assay, CCK-8 cell viability assay, flow cytometry, and caspase-3 activity assay were performed to evaluate the radiosensitization of UBR5 knockdown in NSCLC cells, and the underlying mechanism in vitro was also investigated. UBR5 was highly expressed in NSCLC tissues, and its high expression was associated with the poor prognosis in 50 patients with NSCLC. After X-ray irradiation, the protein expression levels of UBR5 were also increased in NSCLC cells. UBR5 inhibition enhanced the radiosensitivity of NSCLC cells by inhibiting the cell viability and inducing apoptosis. Further investigation indicated that UBR5 knockdown-mediated radiosensitization involved the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. Knockdown of UBR5 radiosensitizes NSCLC cells via the inactivation of the PI3K/AKT signal, which provided a novel therapeutic target for NSCLC radiosensitization.

  • carcinoma

Data availability statement

All data relevant to the study are included in the article or uploaded as supplemental information. All data in this study can be obtained by proper request from the authors.

Statistics from Altmetric.com

Data availability statement

All data relevant to the study are included in the article or uploaded as supplemental information. All data in this study can be obtained by proper request from the authors.

View Full Text

Footnotes

  • Contributors Y-FG conducted most of the experiments, designed the study and wrote the manuscript; X-PG conducted the experiments and analyzed the data. All authors have read and approved the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.