Downregulation of USP32 inhibits cell proliferation, migration and invasion in human small cell lung cancer. (9th June 2017)

• Record Type: Journal Article
• Authors: Hu, Wenyu; Wei, Haiyan; Li, Keming; Li, Pei; Lin, Jiamao; Feng, Rui
• Is Part Of: Cell proliferation. Volume 50:Number 4(2017:Aug.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-06-09
• Subjects: cell apoptosis -- cell cycle -- cell proliferation -- invasion -- small cell lung cancer -- USP32; Cell proliferation -- Periodicals; 571.84
• DOI: 10.1111/cpr.12343
• Languages: English
• ISSNs: 0960-7722

Abstract

Abstract: Objectives: Ubiquitin specific protease 32 ( USP32 ) is a highly conserved but uncharacterized gene, which has been reported to be associated with growth of breast cancer cells. However, the role of USP32 in human small cell lung cancer (SCLC) has not been uncovered. The aim of this study was to investigate and evaluate the clinical significance of USP32 in patients with SCLC. Materials and methods: Expression of USP32 was firstly investigated using public online data sets and then determined in SCLC tissues and cell lines using quantitative real‐time PCR, Western blotting and immunohistochemical staining. SCLC cells were transfected with a small‐interfering RNA targeting USP32 mRNA and analysed for cell viability, proliferation ability, cell cycle distribution, apoptosis and invasion. Results: USP32 was found to be overexpressed in SCLC tissues compared with normal tissues. High USP32 expression was significantly correlated with disease stage and invasion. In vitro experiments demonstrated that silencing of USP32 caused a significant decrease in the proliferation and migration rate of cells. Furthermore, USP32 silencing arrested cell cycle progression at G0/G1 phase via decreasing CDK4/Cyclin D1 complex and elevating p21. In addition, downregulation of USP32 significantly induced cell apoptosis by activating cleaved caspase‐3 and cleaved PARP, as well as inhibiting cell invasiveness via altering epithelial mesenchymal transition expression. Conclusions: Our results suggest for the first time that USP32 is important for SCLC progression and might be a potential target for molecular therapy of SCLC.