Research Papers:

TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer

Yan Yin _, Jun Zhong, Si-Wei Li, Jian-Zhe Li, Min Zhou, Yin Chen, Yi Sang and Lijuan Liu

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Oncotarget. 2016; 7:86755-86765. https://doi.org/10.18632/oncotarget.13550

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Yan Yin1,*, Jun Zhong2,*, Si-Wei Li3,*, Jian-Zhe Li4, Min Zhou1, Yin Chen1, Yi Sang5, Lijuan Liu1

1Department of Pharmacy, Jiangxi Cancer Hospital, Nanchang, China

2Department of Radiotherapy, Jiangxi Cancer Hospital, Nanchang, China

3Department of Radiation Oncology, The Affiliated Hospital of Guilin Medical University, Guilin, China

4Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, China

5Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital, Nanchang University, Nanchang, China

*These authors have contributed equally to this work

Correspondence to:

Lijuan Liu, email: [email protected]

Yi Sang, email: [email protected]

Keywords: TRIM11, colon cancer, miR-24-3p

Received: July 18, 2016     Accepted: November 07, 2016     Published: November 24, 2016


TRIM11 (tripartite motif-containing protein 11) is an E3 ubiquitin ligase recently identified as an oncogene in malignant glioma and lung cancer. In the present study, we report that expression of TRIM11 was increased in colon cancer (CC) tissue relative to paired normal tissues and that higher TRIM11 levels predicted poor overall survival (OS) and disease-free survival (DFS) in CC patients. Mechanistically, we showed that miR-24-3p downregulation contributes to TRIM11 upregulation in CC. We also demonstrated that TRIM11 overexpression promotes cell proliferation and colony formation and inhibits apoptosis in CC, while knocking down TRIM11 using CRISPR/Cas9-mediated genome editing inhibited cell proliferation and induced apoptosis. Silencing TRIM11 in vivo decreased tumor growth. These findings indicate that TRIM11 facilitates CC progression by promoting cell proliferation and inhibiting apoptosis and that the novel miR-24-3p/TRIM11 axis may be a useful new target for treating patients with CC.

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