Kinesin family member 11 depletion suppressed the proliferation of lung adenocarcinoma cells
LENG Ling,MIAO Ling-yue,XU Xia
Department of Respiratory and Critical Care Medicine, Chengyang District People's Hospital of Qingdao City, Qingdao266000, China.
Abstract:
Objective To evaluate the expression level of kinesin family member 11 (KIF11) in human lung adenocarcinoma tissues, and reveal the impact of KIF11 on the progression of lung adenocarcinoma and the possible mechanism. Methods The TCGA database was utilized to assess the expression of KIF11 in lung adenocarcinoma tissues and its correlation with patient prognosis. Immunohistochemical staining was employed to detect the expression level of KIF11 in tumor tissues from lung adenocarcinoma patients, followed by clinicopathological analysis. Colony formation and MTT assays were conducted to evaluate the impact of KIF11 on the proliferation of lung adenocarcinoma cells in vitro. Additionally, animal tumor growth models were established to confirm its effect on the progression of lung adenocarcinoma in vivo. Results Based on the TCGA database and IHC results, the expression of KIF11 is enhanced in human lung adenocarcinoma tissues. The expression of KIF11 correlates with clinicopathological features such as the prognosis of lung adenocarcinoma patients, tumor size (P =0.015), and clinical stage (P =0.028). In vitro studies on A549 and H1975 cells showed that knockdown of KIF11 significantly reduced the number of tumor cell clones, indicating that the growth of tumor cells was inhibited after KIF11 knockdown (P <0.05). Mouse studies also demonstrated that knockdown of KIF11 significantly slowed down the growth rate of tumor cells (P <0.05). KIF11 promotes the proliferation of lung adenocarcinoma cells both in vitro and in vivo. Conclusion We found that KIF11 is significantly overexpressed in human lung adenocarcinoma tissues, confirming its impact on the proliferation and progression of lung adenocarcinoma.
