Downregulation of ubiquitin-specific peptidase 39 suppresses the proliferation and induces the apoptosis of human colorectal cancer cells Corrigendum in /10.3892/ol.2018.9234

Xing,Zhiyuan; Sun,Fengbo; He,Wang; Wang,Zhiwei; Song,Xiuqi; Zhang,Fengjuan

doi:10.3892/ol.2018.8061

Downregulation of ubiquitin-specific peptidase 39 suppresses the proliferation and induces the apoptosis of human colorectal cancer cells

Corrigendum in: /10.3892/ol.2018.9234

Authors:
- Zhiyuan Xing
- Fengbo Sun
- Wang He
- Zhiwei Wang
- Xiuqi Song
- Fengjuan Zhang
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Affiliations: Department of General Surgery, The Second Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong 266000, P.R. China, Department of General Surgery, Qingdao Haici Medical Group, Qingdao, Shandong 266000, P.R. China, Department of Hepatopathy, Qingdao Sixth People's Hospital, Qingdao, Shandong 266000, P.R. China, Department of Infection, The Second Affiliated Hospital of Qingdao University Medical College, Qingdao, Shandong 266000, P.R. China
Published online on: February 15, 2018 https://doi.org/10.3892/ol.2018.8061
Pages: 5443-5450
Copyright: © Xing et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ubiquitin-specific peptidase 39 (USP39) has been reported to participate in the mitotic spindle checkpoint and the process of cytokinesis. and has been identified as a therapeutic target for various types of cancer. However, the effect of USP39 in colorectal cancer (CRC) has not been investigated. To explore the functional role of USP39 in CRC cell growth, lentivirus-mediated RNA interference was applied to inhibit USP39 expression in SW1116 and HCT116 cells. The relative USP39 mRNA and protein expression levels were significantly reduced in the USP39 knockdown cells, as verified by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. USP39 knockdown significantly reduced the proliferation and colony formation abilities of CRC cells, and induced apoptosis and cell cycle arrest in the G2/M phases, as determined by an MTT assay, a colony formation assay and flow cytometry analysis. Furthermore, western blot analysis demonstrated that USP39 knockdown may have induced apoptosis through the upregulation of p53, p‑p53, PARP and caspase‑3 expression in SW1116 cells. In conclusion, USP39 may be a novel biological marker for targeted therapy against CRC, and requires further investigation.

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