Back to Journals » Cancer Management and Research » Volume 11

TRIM14 promotes cell proliferation and inhibits apoptosis by suppressing PTEN in colorectal cancer

Authors Shen W, Jin Z, Tong X, Wang H, Zhuang L, Lu X, Wu S

Received 1 April 2019

Accepted for publication 23 May 2019

Published 24 June 2019 Volume 2019:11 Pages 5725—5735

DOI https://doi.org/10.2147/CMAR.S210782

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 2

Editor who approved publication: Dr Kenan Onel


Weidong Shen,1,* Zhonghai Jin,2,* Xiuping Tong,2 Haiying Wang,2 Lilei Zhuang,2 Xiaofeng Lu,2 Shenbao Wu2

1Department of Gastroenterology, Jiangyin Hospital Affiliated to Nantong University, Jiangyin, People’s Republic of China; 2Department of Gastroenterology, Yiwu Hospital, Wenzhou Medical University, Yiwu, People’s Republic of China

*These authors contributed equally to this work

Background: Colorectal cancer (CRC) is among the most frequent and lethal malignancies worldwide. Although great advances have been made in the treatment of CRC, prognosis remains poor. Our previous study indicated that tripartite motif-containing 14 (TRIM14) was upregulated in CRC samples.
Methods: In the current study, the association between TRIM14 and CRC was investigated. Protein expression was determined by Western blotting and immunohistochemistry. Further, the biological roles of TRIM14 in CRC cell proliferation and apoptosis were explored both in vitro and in vivo.
Results: We observed that increased TRIM14 expression in CRC tissues was closely related with aggressive clinicopathological characteristics and poor prognosis. TRIM14 knockdown markedly reduced proliferation and increased apoptosis in HT-29 and SW620 cells, whereas TRIM14 overexpression in LoVo cells displayed opposite results. Xenograft experiments using HT-29 cells confirmed suppression of tumor growth and induction of apoptosis upon TRIM14 knockdown in vivo. Furthermore, downregulation of TRIM14 inhibited the AKT pathway, as indicated by reduced levels of phosphorylated AKT, Bcl-2 and Cyclin D1, and elevated levels of phosphatase andtensin homology (PTEN) and p27. In addition, TRIM14 colocalized with PTEN in the cytoplasm and induced PTEN ubiquitination. Moreover, PTEN overexpression significantly inhibited pro-proliferative effects of TRIM14, indicating an involvement of PTEN/AKT signaling in mediating TRIM14 functions.
Conclusions: The present data demonstrate that TRIM14 overexpression promotes CRC cell proliferation, suggesting TRIM14 as an attractive therapeutic target for CRC.

Keywords: colorectal cancer, TRIM14, PTEN, AKT


Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]