Overexpression of TRIM66 functions as an oncogene in lung cancer progression

被引:0
作者
Liu, Jialiang [1 ]
Wu, Wanxin [2 ]
Xie, Yonghong [4 ]
Lv, Xiaodong [1 ]
Ling, Danyan [2 ]
Yang, Zhiping [3 ]
机构
[1] Jiaxing Univ, Affiliated Hosp 1, Dept Pneumol, Jiaxing, Zhejiang, Peoples R China
[2] Jiaxing Univ, Affiliated Hosp 1, Dept Pathol, Jiaxing, Zhejiang, Peoples R China
[3] Jiaxing Univ, Affiliated Hosp 1, Dept Oncol 04 F 14, 1882 Zhonghuan South Rd, Jiaxing 314001, Zhejiang, Peoples R China
[4] Jiaxing Univ, Coll Med, Dept Pneumol, Jiaxing, Zhejiang, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2016年 / 9卷 / 05期
关键词
TRIM66; lung cancer; Bcl-2; Bax; EMT pathway; BCL-2; FAMILY; CELL; EPIDEMIOLOGY; SURVEILLANCE; MITOCHONDRIA; INVASION; MMP-9; MATRIX-METALLOPROTEINASE-9; TRANSCRIPTION; METASTASIS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tripartite motif (TRIM) family is identified as an E3 ubiquitin ligases that is implicated in critical progression of cancer. This study was in an effort to reveal the expression and functional mechanisms of TRIM66 in lung cancer. The expression of TRIM66 was examined in lung cancer tissues and two lung cancer cell lines were picked up for further experiments. Effects of silencing TRIM66 on cell proliferation, cell cycle, cell apoptosis and metastasis were analyzed respectively. And relative protein levels of apoptosis and epithelial-to-mesenchymal transition (EMT) pathway were detected using Western blot. Our data suggested that expression of TRIM66 was significantly higher in lung cancer tissues compared to normal tissues. Silencing of TRIM66 repressed proliferation, cell cycle and metastasis, but facilitated cell apoptosis of lung cancer cell lines. Suppressed Bcl-2 and promoted Bax, caspase3 and caspase9 were examined in TRIM66 silencing cells. Additionally, the proteins related to EMT pathway including MMP-2, MMP-9, Snail and Twist, was inhibited by TRIM66 knocking down. In conclusion, our study demonstrated that TRIM66 was highly expressed in lung cancer, and functioned as an oncogene in lung cancer development.
引用
收藏
页码:4966 / 4977
页数:12
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