Overexpression of anillin is related to poor prognosis in patients with hepatocellular carcinoma

作     者：Long-Hui Zhang Dong Wang Zhao Li Gang Wang Ding-Bao Chen Qian Cheng Shi-Hua Hu Ji-Ye Zhu Long-Hui Zhang;Dong Wang;Zhao Li;Gang Wang;Ding-Bao Chen;Qian Cheng;Shi-Hua Hu;Ji-Ye Zhu

作者机构：Department of Hepatobiliary SurgeryPeking University People’s HospitalBeijing 100044China Peking University Institute for Organ TransplantationBeijing 100044China Beijing Key Laboratory of Liver Cirrhosis and Liver CancerBeijing 100044China Department of PathologyPeking University People’s HospitalBeijing 100044China 

出 版 物：《Hepatobiliary & Pancreatic Diseases International》 (国际肝胆胰疾病杂志（英文版）)

年 卷 期：2021年第20卷第4期

页      面：337-344页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：This study was supported by the grants from National Natural Science Foundation of China(81570590 and 81502509) 

主　　题：Anillin DNA methylation Copy number variation Hepatocellular carcinoma Prognosis 

摘      要：Background: Anillin(ANLN) is required for tumor growth. It has been proven that knockdown of ANLN effectively reduces the occurrence of hepatocellular carcinoma(HCC) in transgenic mice. However, the functional role of ANLN in HCC patients remains to be elucidated. Methods: Both microarray and TCGA project were used for the analyses of ANLN expression and regulation in HCC. The effect of ANLN on proliferation and cell cycle was detected by CCK-8, colony formation assay and flow cytometry. ANLN expression was measured by immunohistochemistry. Correlation between ANLN expression and clinicopathological features was assessed by Pearson Chi-square test and 5-year overall survival after liver resection was evaluated by Kaplan–Meier method. Results: Increased copy number, decreased methylation levels in the Cp G island and upregulated histone hypermethylation of ANLN were found in HCC. Knockdown of ANLN inhibited proliferation and induced G2/M phase arrest in SMMC-7721 cells. ANLN was mainly expressed in the nucleus and showed significantly higher expression levels in cancerous tissues than those in paired adjacent tissues. Moreover, nuclear ANLN expression levels in HCC metastases were significantly higher than those in primary HCC. The results of Cox proportional hazards regression model suggested that ANLN nuclear expression in HCC was an independent risk factor for poor 5-year overall survival of patients after liver resection. Conclusions: ANLN is a potential therapeutic target for HCC. Patients with nuclear ANLN overexpression in HCC tissue may need adjuvant therapy after liver resection.