Stathmin overexpression is associated with growth, invasion and metastasis of lung adenocarcinoma

// Lin Yurong 1 , Rong Biaoxue 1 , Li Wei 1 , Ming Zongjuan 1 , Shi Hongyang 1 , Fang Ping 1 , Gao Wenlong 2 , Yang Shuanying 1 , Li Zongfang 3 1 Department of Respiratory Medicine, Second Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China 2 Department of Statistics and Epidemiology, Medical College, Lanzhou University, Lanzhou, China 3 Department of Elderly Surgery, Second Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China Correspondence to: Yang Shuanying, email: yangshuanying66@126.com , yangshuanying66@163.com Keywords: stathmin, lung adenocarcinoma, shRNA, tumor growth, proliferation Received: February 21, 2016     Accepted: July 09, 2016     Published: August 02, 2016 ABSTRACT Stathmin has been investigated as a tumor biomarker because it appear to be associated with tumorigenesis; however, the effect of stathmin in lung adenocarcinoma (LAC) remains poorly understood. The purpose of this study was to examine the expression of stathmin in lung adenocarcinoma, and to disclose the relationship between them. The expression of stathmin was examined by RT-PCR, IHC and Western blot. Furthermore, small interfering RNA (shRNA)-mediated silencing of stathmin was employed in LAC cells to investigate cell proliferation, invasion and apoptosis. In this study, we showed that overexpression of stathmin was significantly associated with poorly differentiated, lymph node metastasis and advance TNM stages of lung adenocarcinoma. And silencing of stathmin expression inhibited the proliferation, migration and invasion of lung adenocarcinoma PC-9 cells, and retarded the growth of PC-9 cells xenografts in nude mice. Additionally, the anticarcinogenic efficacy of stathmin silencing might be involved in P38 and MMP2 signaling pathways. In conclusion, these results showed that stathmin expression was significantly up-regulated in LAC, which may act as a biomarker for LAC. Furthermore, silence of stathmin inhibiting LAC cell growth indicated that stathmin may be a promising molecular target for LAC therapy.