Jing Hu1, Dongdong Yang2, Huijuan Zhang3, Wei Liu3, Yanbin Zhao3, Hailing Lu3, Qingwei Meng3, Hui Pang3, Xuesong Chen3, Yanlong Liu4, Li Cai5. 1. The 4th Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China. Electronic address: hujing@ems.hrbmu.edu.cn. 2. Department of Oncological Surgery, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. 3. The 4th Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China. 4. Department of Colorectal Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China. Electronic address: liuyanlong1979@163.com. 5. The 4th Department of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China. Electronic address: caili@ems.hrbmu.edu.cn.
Abstract
OBJECTIVES: Our previous study showed that USP22 as an oncogene may mediate cancer development and progression in NSCLC, but the underlying molecular mechanism remains uncharacterized. Epithelial-mesenchymal transition (EMT) has been reported to play an important role in migration and invasion of the tumor cells. Thus, this study aims to determine the clinical significance and the possible roles of USP22 in EMT and progression of lung adenocarcinoma. METHODS: Immunohistochemistry was used to determine the expression of USP22 in clinical samples. The clinical correlations and prognostic significance of the aberrantly expressed proteins were evaluated by statistical analysis. Moreover, we evaluated whether USP22 could induce EMT in cultured lung cancer cells. RESULTS: The USP22 expression was positive in 76.03% of specimens and was correlated with advanced clinicopathologic classifications (differentiation, T and AJCC stages) and TGF-β1 expression (p=0.008). Multivariate Cox regression analysis revealed that USP22 expression level was an independent prognostic factor for both overall survival and disease-free survival (HR, 2.060; p=0.013 and HR, 1.993; p=0.016). In vitro study revealed that USP22 can regulate proliferation and invasive properties, and induce EMT of lung adenocarcinoma cells. Moreover, USP22 may up-regulate TGF-β1 expression. CONCLUSIONS: Our data indicated that USP22 may promote lung adenocarcinoma cell invasion by the induction of EMT.
OBJECTIVES: Our previous study showed that USP22 as an oncogene may mediate cancer development and progression in NSCLC, but the underlying molecular mechanism remains uncharacterized. Epithelial-mesenchymal transition (EMT) has been reported to play an important role in migration and invasion of the tumor cells. Thus, this study aims to determine the clinical significance and the possible roles of USP22 in EMT and progression of lung adenocarcinoma. METHODS: Immunohistochemistry was used to determine the expression of USP22 in clinical samples. The clinical correlations and prognostic significance of the aberrantly expressed proteins were evaluated by statistical analysis. Moreover, we evaluated whether USP22 could induce EMT in cultured lung cancer cells. RESULTS: The USP22 expression was positive in 76.03% of specimens and was correlated with advanced clinicopathologic classifications (differentiation, T and AJCC stages) and TGF-β1 expression (p=0.008). Multivariate Cox regression analysis revealed that USP22 expression level was an independent prognostic factor for both overall survival and disease-free survival (HR, 2.060; p=0.013 and HR, 1.993; p=0.016). In vitro study revealed that USP22 can regulate proliferation and invasive properties, and induce EMT of lung adenocarcinoma cells. Moreover, USP22 may up-regulate TGF-β1 expression. CONCLUSIONS: Our data indicated that USP22 may promote lung adenocarcinoma cell invasion by the induction of EMT.
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