Knockdown of TRIM65 inhibits lung cancer cell proliferation, migration and invasion: A therapeutic target in human lung cancer.
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.
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Xiao-Lin
XL
Wang
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Wei-Ping
WP
Shi
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Hong-Can
HC
Shi
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Shi-Chun
SC
Lu
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Kang
K
Wang
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Chao
C
Sun
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Jian-Sheng
JS
He
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Wei-Guo
WG
Jin
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Xiao-Xia
XX
Lv
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Hui
H
Zou
Department of Thoracic Surgery, Northern Jiangsu People's Hospital and Clinical Medical College of Yangzhou University, Yangzhou 225001, People's Republic of China.
Yu-Sheng
YS
Shu
TRIM65; apoptosis; lung cancer; migration