Open AccessDownregulation of USP 32 inhibits cell proliferation, migration and invasion in human small cell lung cancer
Author(s) -
Hu Wenyu,
Wei Haiyan,
Li Keming,
Li Pei,
Lin Jiamao,
Feng Rui
Publication year - 2017
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12343
Subject(s) - cell growth , biology , cell cycle , cancer research , downregulation and upregulation , gene silencing , cyclin d1 , viability assay , apoptosis , transfection , cell , small interfering rna , microbiology and biotechnology , cell culture , gene , genetics , biochemistry
Objectives Ubiquitin specific protease 32 ( USP 32 ) is a highly conserved but uncharacterized gene, which has been reported to be associated with growth of breast cancer cells. However, the role of USP 32 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 USP 32 in patients with SCLC . Materials and methods Expression of USP 32 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 USP 32 mRNA and analysed for cell viability, proliferation ability, cell cycle distribution, apoptosis and invasion. Results USP 32 was found to be overexpressed in SCLC tissues compared with normal tissues. High USP 32 expression was significantly correlated with disease stage and invasion. In vitro experiments demonstrated that silencing of USP 32 caused a significant decrease in the proliferation and migration rate of cells. Furthermore, USP 32 silencing arrested cell cycle progression at G0/G1 phase via decreasing CDK 4/Cyclin D1 complex and elevating p21. In addition, downregulation of USP 32 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 USP 32 is important for SCLC progression and might be a potential target for molecular therapy of SCLC .