Identification of Pannexin 2 as a Novel Marker Correlating with Ferroptosis and Malignant Phenotypes of Prostate Cancer Cells

• Published in: OncoTargets and therapy 2020-01, Vol.13, p.4411-4421
• Main Authors: Liao, Duwu, Yang, Guang, Yang, Yuan, Tang, Xueyong, Huang, Haixia, Shao, Jichun, Pan, Qi
• Format: Article
• Language: English
• Subjects: Original Research
• ISSN: 1178-6930; 1178-6930
• DOI: 10.2147/OTT.S249752

Prostate cancer (PCa) is a widespread urinary neoplasm and one of the most prevalent and second most frequent malignancies diagnosed in males worldwide. This study aimed to identify a candidate marker and explore its molecular mechanism in PCa. Gene expression datasets, GSE55945 (n=21) and GSE46602 (n=50), were downloaded from the Gene Expression Omnibus database. Bioinformatic approaches were applied to identify potential markers. Effects of the candidate marker on proliferation, migration, invasion, and ferroptosis (ferrous iron and malondialdehyde (MDA)) in PCa cells and its mechanism were assessed after performing cell transfection. A total of 1435 common differentially expressed genes were identified in GSE55945 and GSE46602. Five key gene modules were listed based on a protein-protein interaction network, containing five hub genes. Pannexin 2 ( ), a candidate marker was identified, and findings revealed substantial upregulation of its expression levels in PCa cell lines. Blocking expression of resulted in suppression of proliferation, migration, and invasion in PCa cells, while increasing ferrous iron and MDA levels. However, these effects were rescued by activator, oltipraz. The signaling pathway was consequently applied to determine underlying mechanism of in PCa cells. We established that silencing remarkably reduced protein expression levels in members of signaling pathway ( and ). Our study demonstrated that is implicated in the pathogenesis of PCa, which regulates malignant phenotypes and ferroptosis through signaling pathway, and maybe a potential therapeutic target for PCa.