GPX8 promotes migration and invasion by regulating epithelial characteristics in non‐small cell lung cancer

Background Non‐small cell lung cancer (NSCLC) is the most common cause of cancer‐related death worldwide. The family of glutathione peroxidase (GPX), an important antioxidant enzyme in human tissues, has been discovered to play a key role in the development of cancers. GPX8 is the most promising mol...

Full description

Bibliographic Details
Main Authors: Jun Zhang, Yun Liu, Yan Guo, Qiang Zhao
Format: Article
Language:English
Published: Wiley 2020-11-01
Series:Thoracic Cancer
Subjects:
Online Access:https://doi.org/10.1111/1759-7714.13671
Description
Summary:Background Non‐small cell lung cancer (NSCLC) is the most common cause of cancer‐related death worldwide. The family of glutathione peroxidase (GPX), an important antioxidant enzyme in human tissues, has been discovered to play a key role in the development of cancers. GPX8 is the most promising molecule of the family in a therapeutic strategy against a variety of cancers. The main purpose of this study was to examine and analyze the function and clinical value of GPX8 in NSCLC. Methods Immunohistochemistry (IHC), western blot analysis and quantitative real‐time polymerase chain reaction (qPCR) were used to assess GPX8 expression and its clinical significance in NSCLC. A series of cell biology experiments and bioinformatic analysis tools were further used to study the function of GPX8. Results GPX8 expression in tumor tissues was much higher than that in normal lung tissues. High expression of GPX8 in NSCLC was correlated with a worse clinical outcome and prognosis. Furthermore, GPX8 could inhibit the apoptosis of tumor cells and promote its migration and invasion. Conclusions Our results conclusively demonstrated that GPX8 could affect the oncogenesis and prognosis of NSCLC via regulating epithelial characteristics. The study also illustrated that GPX8 could serve as a prognostic predictor and potential therapeutic target for NSCLC.
ISSN:1759-7706
1759-7714