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      TRIM52 promotes colorectal cancer cell proliferation through the STAT3 signaling

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          Abstract

          Background

          The tripartite motif (TRIM) family proteins are implicated in the pathogenesis of various human malignancies. The up-regulation and oncogenic roles of TRIM52 have been reported in hepatocellular carcinoma. In the current study, we aimed to examine its expression and possible function in colorectal cancer (CRC).

          Method

          Immunohistochemical staining or immunoblotting analysis was carried out to detect protein expression. Cell proliferation and apoptosis was evaluated by Cell Counting Kit-8 (CCK-8) and flow cytometry assay, respectively.

          Results

          TRIM52 expression was increased in 67.5% of CRC tissues (54/80) compared to matched normal colonic mucosa. TRIM52 expression was closely related with tumor size ( p = 0.0376), tumor stage ( p = 0.0227) and overall survival ( p = 0.0177). Short hairpin RNAs (shRNAs) targeting TRIM52 had the potential anti-proliferative effects on CRC cell lines, SW480 and LoVo, by inducing cell apoptosis. In addition, an in vivo xenograft experiment confirmed the in vitro results. In addition, TRIM52 shRNAs decreased the phosphorylation of STAT3, but increased the protein expression of SHP2, a negative regulator of STAT3 phosphorylation. TRIM52 formed a complex with SHP2 and promoted the ubiquitination of SHP2. Furthermore, inhibition of the STAT3 signaling by AG490 in RKO cells significantly abolished the effects of TRIM52 overexpression on cell proliferation, apoptosis and STAT3 activation.

          Conclusions

          TRIM52 might exert oncogenic role in CRC via regulating the STAT3 signaling pathway.

          Electronic supplementary material

          The online version of this article (10.1186/s12935-019-0775-4) contains supplementary material, which is available to authorized users.

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          Most cited references27

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          TRIM proteins and diseases.

          Masashi Watanabe, Shigetsugu Hatakeyama (2017)
          Ubiquitination is one of the posttranslational modifications that regulates a number of intracellular events including signal transduction, protein quality control, transcription, cell cycle, apoptosis and development. The ubiquitin system functions as a garbage machine to degrade target proteins and as a regulator for several signalling pathways. Biochemical reaction of ubiquitination requires several enzymes including E1, E2 and E3, and E3 ubiquitin ligases play roles as receptors for recognizing target proteins. Most of the tripartite motif (TRIM) proteins are E3 ubiquitin ligases. Recent studies have shown that some TRIM proteins function as important regulators for a variety of diseases including cancer, inflammatory diseases, infectious diseases, neuropsychiatric disorders, chromosomal abnormalities and developmental diseases. In this review, we summarize the involvement of TRIM proteins in the aetiology of various diseases.
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            PTP1B: a double agent in metabolism and oncogenesis.

            Shu-Chin Yip, Sayanti Saha, Jonathan Chernoff (2010)
            PTP1B, a non-transmembrane protein tyrosine phosphatase that has long been studied as a negative regulator of insulin and leptin signaling, has received renewed attention as an unexpected positive factor in tumorigenesis. Here, we highlight how views of this enzyme have evolved from regarding it as a simple metabolic off-switch to a more complex view of PTP1B as an enzyme that can play both negative and positive roles in diverse signaling pathways. These dual characteristics make PTP1B a particularly attractive therapeutic target for diabetes, obesity, and perhaps breast cancer. Copyright 2010 Elsevier Ltd. All rights reserved.
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              Inhibition of JAK1, 2/STAT3 signaling induces apoptosis, cell cycle arrest, and reduces tumor cell invasion in colorectal cancer cells.

              Ying Chen, Gang Zhang, Feng Sun … (2008)
              Abnormalities in the STAT3 pathway are involved in the oncogenesis of several cancers. However, the mechanism by which dysregulated STAT3 signaling contributes to the progression of human colorectal cancer (CRC) has not been elucidated, nor has the role of JAK, the physiological activator of STAT3, been evaluated. To investigate the role of both JAK and STAT3 in CRC progression, we inhibited JAK with AG490 and depleted STAT3 with a SiRNA. Our results demonstrate that STAT3 and both JAK1 and 2 are involved in CRC cell growth, survival, invasion, and migration through regulation of gene expression, such as Bcl-2, p1(6ink4a), p21(waf1/cip1), p27(kip1), E-cadherin, VEGF, and MMPs. Importantly, the FAK is not required for STAT3-mediated regulation, but does function downstream of JAK. In addition, our data show that proteasome-mediated proteolysis promotes dephosphorylation of the JAK2, and consequently, negatively regulates STAT3 signaling in CRC. Moreover, immunohistochemical staining reveals that nuclear staining of phospho-STAT3 mostly presents in adenomas and adenocarcinomas, and a positive correlation is found between phospho-JAK2 immunoreactivity and the differentiation of colorectal adenocarcinomas. Therefore, our findings illustrate the biologic significance of JAK1, 2/STAT3 signaling in CRC progression and provide novel evidence that the JAK/STAT3 pathway may be a new potential target for therapy of CRC.
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                Author and article information

                Contributors
                Shengli Pan: 86-21-3484588 , slpandoctor@163.com
                Yingying Deng: 360728217@qq.com
                Jun Fu: carrie@hotmail.com.cn
                Yuhao Zhang: openmouse@126.com
                Zhijin Zhang: greatjin@163.com
                Xiaokun Ru: xiaokun_1013@163.com
                Xianju Qin: 86-21-3484588 , qinxj@hotmail.com
                Journal
                Journal ID (nlm-ta): Cancer Cell Int
                Journal ID (iso-abbrev): Cancer Cell Int
                Title: Cancer Cell International
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1475-2867
                Publication date (Electronic): 14 March 2019
                Publication date PMC-release: 14 March 2019
                Publication date Collection: 2019
                Volume: 19
                Electronic Location Identifier: 57
                Affiliations
                [1 ]Division of Gastrointestinal Surgery, Department of General Surgery, Shanghai Eighth People’s Hospital, No. 8 Caobao Road, Xuhui District, Shanghai, 200232 China
                [2 ]Department of Ophtalmology, Shanghai Eighth People’s Hospital, Shanghai, China
                Article
                Publisher ID: 775
                DOI: 10.1186/s12935-019-0775-4
                PMC ID: 6419475
                PubMed ID: 30918473
                SO-VID: dc6e156f-ddf3-4d72-b6b5-89002eacd019
                Copyright © © The Author(s) 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 23 October 2018
                Date accepted : 8 March 2019
                Funding
                Funded by: Foundation of Shanghai Municipal Commission of Health and Family Planning (CN)
                Award ID: (201740229)
                Award Recipient :
                Categories
                Subject: Primary Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: trim52,proliferation,prognosis,stat3
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: trim52, proliferation, prognosis, stat3

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