Knockdown of TRIM65 inhibits lung cancer cell proliferation, migration and invasion: A therapeutic target in human lung cancer

作者：Xiaolin Wang, Weiping Shi, Hongcan Shi, Shichun Lu, Kang Wang, Chao Sun, Jian-Sheng He, Weiguo Jin, Xiaoxia Lv, Hui Zou, Yusheng Shu · 发表于：Oncotarget · 年份：2016 · DOI：10.18632/oncotarget.13131 · 被引用次数：30 · 研究领域：interferon and immune responses、Cancer Mechanisms and Therapy、Signaling Pathways in Disease

// Xiao-Lin Wang 1 , Wei-Ping Shi 1 , Hong-Can Shi 1 , Shi-Chun Lu 1 , Kang Wang 1 , Chao Sun 1 , Jian-Sheng He 1 , Wei-Guo Jin 1 , Xiao-Xia Lv 1 , Hui Zou 1 , Yu-Sheng Shu 1 1 Department of Thoracic Surgery, Northern Jiangsu People’s Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People’s Republic of China Correspondence to: Yu-Sheng Shu, email: shuyu_sheng@163.com Keywords: lung cancer, TRIM65, apoptosis, migration Received: July 28, 2016      Accepted: October 19, 2016      Published: November 05, 2016 ABSTRACT Lung cancer is the most commonly diagnosed type of cancer worldwide. Although TRIM65 is an important protein involved in white matter lesion, the role of TRIM65 in human cancer remains less understood. Here, we reported that TRIM65 was significantly overexpressed in lung cancer tissues compared with adjacent normal lung tissues. Furthermore, TRIM65 expression was closely related to overall survival of patients with lung cancer. Knock down of TRIM65 in two lung cancer cell lines, SPC-A-1 and NCI-H358, resulted in a significant reduction in cell proliferation, migration, invasion and adhesion and a dramatic increase in G0-G1 phase arrest and apoptosis. In vivo tumorigenesis experiment also revealed that depletion of TRIM65 expression inhibited NCI-H358 cell growth. Moreover, based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found tha...