已发表论文

TRIM11 通过靶向 AKT/GLUT1 通路促进乳腺癌细胞的增殖和糖酵解

 

Authors Song W, Wang Z, Gu X, Wang A, Chen X, Miao H, Chu J, Tian Y

Received 5 March 2019

Accepted for publication 16 May 2019

Published 28 June 2019 Volume 2019:12 Pages 4975—4984

DOI https://doi.org/10.2147/OTT.S207723

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Rachel Predeepa

Peer reviewer comments 2

Editor who approved publication: Dr William Cho

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.
Keywords: breast cancer, TRIM11, AKT, GLUT1, HKII




Figure 2 Knockdown and overexpression of TRIM11 in breast cancer cells.