Knockdown of TRIM65 inhibits lung cancer cell proliferation, migration and invasion: A therapeutic target in human lung cancer
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Xiao-Lin Wang1, Wei-Ping Shi1, Hong-Can Shi1, Shi-Chun Lu1, Kang Wang1, Chao Sun1, Jian-Sheng He1, Wei-Guo Jin1, Xiao-Xia Lv1, Hui Zou1, Yu-Sheng Shu1
1Department of Thoracic Surgery, Northern Jiangsu People’s Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People’s Republic of China
Yu-Sheng Shu, email: [email protected]
Keywords: lung cancer, TRIM65, apoptosis, migration
Received: July 28, 2016 Accepted: October 19, 2016 Published: November 05, 2016
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 that TRIM65 was positive related to cell cycle, metastasis up and RHOA-REG pathways, which was further validated by RT-PCR and Western blot in TRIM65 knockdown lung cancer cells and indicated a possible mechanism underlying its effects on lung cancer. In summary, our study suggests that TRIM65 may work as an oncogene and a new effective therapeutic target for lung cancer treatment.
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