Knockdown of Upregulated Gene 11 (URG11) Inhibits Proliferation, Invasion, and β-Catenin Expression in Non-Small Cell Lung Cancer Cells
Zheliang Liu, Jiao Wu, Lin-xian Wang, Jinfeng Yang, Gaoming Xiao, Huiping Sun, Yue-jun Chen
Abstract
Zheliang Liu, Jiao Wu, Lin-xian Wang, Jinfeng Yang, Gaoming Xiao, Huiping Sun, Yue-jun Chen
Abstract
Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, was found to be involved in the development and progression of several tumors. However, the role of URG11 in human non-small cell lung cancer (NSCLC) has not yet been determined. Therefore, the aim of the present study was to explore the role of URG11 in human NSCLC. Our results found that URG11 was highly expressed in human NSCLC tissues compared with matched normal lung tissues, and higher levels were found in NSCLC cell lines in comparison to the normal lung cell line. Moreover, we also found that knockdown of URG11 significantly inhibited proliferation, migration/invasion of NSCLC cells, as well as suppressed tumor growth in vivo. Furthermore, knockdown of URG11 suppressed the expression of β-catenin, c-Myc, and cyclin D1 in NSCLC cells. Taken together, the study reported here provided evidence that URG11 downregulation suppresses proliferation, invasion, and β-catenin expression in NSCLC cells. Thus, URG11 may be a novel potential therapeutic target for NSCLC.
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Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, was found to be involved in the development and progression of several tumors. However, the role of URG11 in human non-small cell lung cancer (NSCLC) has not yet been determined. Therefore, the aim of the present study was to explore the role of URG11 in human NSCLC. Our results found that URG11 was highly expressed in human NSCLC tissues compared with matched normal lung tissues, and higher levels were found in NSCLC cell lines in comparison to the normal lung cell line. Moreover, we also found that knockdown of URG11 significantly inhibited proliferation, migration/invasion of NSCLC cells, as well as suppressed tumor growth in vivo. Furthermore, knockdown of URG11 suppressed the expression of β-catenin, c-Myc, and cyclin D1 in NSCLC cells. Taken together, the study reported here provided evidence that URG11 downregulation suppresses proliferation, invasion, and β-catenin expression in NSCLC cells. Thus, URG11 may be a novel potential therapeutic target for NSCLC.
Key concepts: Gene knockdown, Downregulation and upregulation, Cancer research, Cyclin D1, Cell growth, Biology, Lung cancer, Cell culture