TRIM11 promotes proliferation and glycolysis of breast cancer cells via targeting AKT/GLUT1 pathway

被引:31
|
作者
Song, Wenbo [1 ,2 ]
Wang, Zheng [3 ]
Gu, Xiang [2 ]
Wang, Ali [2 ]
Chen, XiaoJun [2 ]
Miao, Hui [4 ]
Chu, JunFeng [2 ]
Tian, Ye [5 ]
机构
[1] Soochow Univ, Affiliated Hosp 2, Dept Radiotherapy & Oncol, Suzhou 215004, Peoples R China
[2] Jiangdu Peoples Hosp Yangzhou, Dept Radiotherapy, Dongfanghong Rd 9, Yangzhou 225200, Jiangsu, Peoples R China
[3] Yangzhou Univ, Clin Med Coll, Yangzhou 225200, Jiangsu, Peoples R China
[4] Xuzhou Canc Hosp, Dept Radiotherapy, Xuzhou 221000, Jiangsu, Peoples R China
[5] Soochow Univ, Affiliated Hosp 2, Dept Radiotherapy & Oncol, San Xiang Rd 1055, Suzhou 215004, Jiangsu, Peoples R China
来源
ONCOTARGETS AND THERAPY | 2019年 / 12卷
关键词
breast cancer; TRIM11; AKT; GLUT1; HKII; HEPATOCELLULAR-CARCINOMA; HEXOKINASE II; GLUT1; INVASION; INHIBITION; EXPRESSION; MIGRATION;
D O I
10.2147/OTT.S207723
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background: Tripartite motif-containing protein 11 (TRIM11) is one of the E3 ubiquitin ligases, which is upregulated in several human tumors. Meanwhile, the detailed function of TRIM11 remains unclear in breast cancer cells. Purpose: The purpose of the present study is to analyze the biological function of TRIM11 and identify its potential signaling pathway in breast cancer cells. Patients and methods: Thirty five pairs of breast cancer specimens and adjacent-matched noncancerous samples were used to analyse the expression profile of TRIM11. RNA interference was utilized to silence TRIM11 in three breast cancer cell lines (T47D, ZR7530, and BT474) respectively. Meanwhile, overexpression of TRIM11 was induced in one breast cancer cells (MDA-MB-231) by using Lentiviral vector. Moreover, the AKT inhibitor (MK-2206) was used to determine the correlation between TRIM11 and AKT in breast cancer cells. Results: Our results indicated that TRIM11 was increased in breast cancer tissues. Moreover, TRIM11 was a pro-proliferation regulator in breast cancer cells and participated in the metabolism of glycolysis. Importantly, our results demonstrated that TRIM11 was involved in the AKT/GLUT1 signaling pathway in breast cancer cells. Conclusion: Present research not only gained a deep understanding of the biological function of TRIM11 but also provided evidences to indicate its possible signaling pathway in breast cancer cells.
引用
收藏
页码:4975 / 4984
页数:10
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