TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway

Sun,Ye; Ji,Bing; Feng,Yifei; Zhang,Yue; Ji,Dongjian; Zhu,Chunyan; Wang,Sen; Zhang,Chuan; Zhang,Dongsheng; Sun,Yueming

doi:10.3892/or.2017.5654

TRIM59 facilitates the proliferation of colorectal cancer and promotes metastasis via the PI3K/AKT pathway

Authors:
- Ye Sun
- Bing Ji
- Yifei Feng
- Yue Zhang
- Dongjian Ji
- Chunyan Zhu
- Sen Wang
- Chuan Zhang
- Dongsheng Zhang
- Yueming Sun
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Affiliations: Department of Colorectal Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China
Published online on: May 22, 2017 https://doi.org/10.3892/or.2017.5654
Pages: 43-52
Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Tripartite motif-containing 59 (TRIM59) belongs to the tripartite motif (TRIM) protein family and is upregulated in various malignancies. However, its expression in colorectal cancer (CRC) is still unknown. In the present study, we examined the expression and biological function of TRIM59 in CRC. We analyzed CRC tissues and cells by quantitative real-time polymerase chain reaction. Kaplan-Meier survival analysis was used to evaluate the prognostic significance of TRIM59 in CRC patients. Furthermore, we investigated the role of TRIM59 in CRC growth and metastasis. The potential mechanism underlying the regulation of cell metastasis by TRIM59 was determined by western blotting. TRIM59 expression was conspicuously overexpressed in CRC tissues and CRC cell lines compared to that noted in the corresponding normal control cells. Patients with higher TRIM59 expression had poorer prognosis. Furthermore, knockdown of TRIM59 suppressed cell proliferation through the induction of apoptosis and inhibited migration and invasion significantly in vitro. Further investigation revealed that knockdown of TRIM59 effectively reversed the expression of epithelial-mesenchymal transformation‑related proteins vimentin, Snail and E-cadherin. Our preliminary results confirm that TRIM59 can be mediated by PI3K/AKT signaling. TRIM59 functions as an oncogene in CRC progression, which could be a novel target for the detection and treatment of CRC.

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