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      • Record: found
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      LncRNA MT1JP functions as a ceRNA in regulating FBXW7 through competitively binding to miR-92a-3p in gastric cancer

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          Abstract

          Background

          Emerging evidence has shown that dysregulation function of long non-coding RNAs (lncRNAs) implicated in gastric cancer (GC). However, the role of the differentially expressed lncRNAs in GC has not fully explained.

          Methods

          LncRNA expression profiles were determined by lncRNA microarray in five pairs of normal and GC tissues, further validated in another 75 paired tissues by quantitative real-time PCR (qRT-PCR). Overexpression of lncRNA MT1JP was conducted to assess the effect of MT1JP in vitro and in vivo. The biological functions were demonstrated by luciferase reporter assay, western blotting and rescue experiments.

          Results

          LncRNA MT1JP was significantly lower in GC tissues than adjacent normal tissues, and higher MT1JP was remarkably related to lymph node metastasis and advance stage. Besides, GC patients with higher MT1JP expression had a well survival. Functionally, overexpression of lncRNA MT1JP inhibited cell proliferation, migration, invasion and promoted cell apoptosis in vitro, and inhibited tumor growth and metastasis in vivo. Functional analysis showed that lncRNA MT1JP regulated FBXW7 expression by competitively binding to miR-92a-3p. MiR-92a-3p and down-regulated FBXW7 reversed cell phenotypes caused by lncRNA MT1JP by rescue analysis.

          Conclusion

          MT1JP, a down-regulated lncRNA in GC, was associated with malignant tumor phenotypes and survival of GC. MT1JP regulated the progression of GC by functioning as a competing endogenous RNA (ceRNA) to competitively bind to miR-92a-3p and regulate FBXW7 expression. Our study provided new insight into the post-transcriptional regulation mechanism of lncRNA MT1JP, and suggested that MT1JP may act as a potential therapeutic target and prognosis biomarker for GC.

          Electronic supplementary material

          The online version of this article (10.1186/s12943-018-0829-6) contains supplementary material, which is available to authorized users.

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          Most cited references18

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          FBW7 ubiquitin ligase: a tumour suppressor at the crossroads of cell division, growth and differentiation.

          Markus Welcker, Bruce Clurman (2008)
          FBW7 (F-box and WD repeat domain-containing 7) is the substrate recognition component of an evolutionary conserved SCF (complex of SKP1, CUL1 and F-box protein)-type ubiquitin ligase. SCF(FBW7) degrades several proto-oncogenes that function in cellular growth and division pathways, including MYC, cyclin E, Notch and JUN. FBW7 is also a tumour suppressor, the regulatory network of which is perturbed in many human malignancies. Numerous cancer-associated mutations in FBW7 and its substrates have been identified, and loss of FBW7 function causes chromosomal instability and tumorigenesis. This Review focuses on structural and functional aspects of FBW7 and its role in the development of cancer.
          Article 0 comments Cited 369 times – based on 0 reviews     Review now
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            Long noncoding RNA associated-competing endogenous RNAs in gastric cancer

            Tian Xia, Qi Liao, Xiaoming Jiang … (2014)
            Some long noncoding RNAs (lncRNAs) play important roles in the regulation of gene expression by acting as competing endogenous RNAs (ceRNAs). However, the roles of lncRNA associated-ceRNAs in oncogenesis are not fully understood. Here, based on lncRNA microarray data of gastric cancer, bioinformatic algorithm miRcode and microRNA (miRNA) targets database TarBase, we first constructed an lncRNA-miRNA-mRNA network. Then, we confirmed it by data of six types of other cancer including head and neck squamous cell carcinoma, prostate cancer, papillary thyroid carcinoma, pituitary gonadotrope tumors, ovarian cancer, and chronic lymphocytic leukemia. The results showed a clear cancer-associated ceRNA network. Eight lncRNAs (AC009499.1, GACAT1, GACAT3, H19, LINC00152, AP000288.2, FER1L4, and RP4-620F22.3) and nine miRNAs (miR-18a-5p, miR-18b-5p, miR-19a-3p, miR-20b-5p, miR-106a-5p, miR-106b-5p, miR-31-5p, miR-139-5p, and miR-195-5p) were involved. For instance, through its miRNA response elements (MREs) to compete for miR-106a-5p, lncRNA-FER1L4 regulates the expression of PTEN, RB1, RUNX1, VEGFA, CDKN1A, E2F1, HIPK3, IL-10, and PAK7. Furthermore, cellular experimental results indicated that FER1L4-small interfering RNA (siRNA) simultaneously suppressed FER1L4 and RB1 mRNA level. These results suggest that lncRNAs harbor MREs and play important roles in post-transcriptional regulation in cancer.
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              FBXW7/hCDC4 is a general tumor suppressor in human cancer.

              Olle Sangfelt, Natalie von der Lehr, Sophia Apostolidou … (2007)
              The ubiquitin-proteasome system is a major regulatory pathway of protein degradation and plays an important role in cellular division. Fbxw7 (or hCdc4), a member of the F-box family of proteins, which are substrate recognition components of the multisubunit ubiquitin ligase SCF (Skp1-Cdc53/Cullin-F-box-protein), has been shown to mediate the ubiquitin-dependent proteolysis of several oncoproteins including cyclin E1, c-Myc, c-Jun, and Notch. The oncogenic potential of Fbxw7 substrates, frequent allelic loss in human cancers, and demonstration that mutation of FBXW7 cooperates with p53 in mouse tumorigenesis have suggested that Fbxw7 could function as a tumor suppressor in human cancer. Here, we carry out an extensive genetic screen of primary tumors to evaluate the role of FBXW7 as a tumor suppressor in human tumorigenesis. Our results indicate that FBXW7 is inactivated by mutation in diverse human cancer types with an overall mutation frequency of approximately 6%. The highest mutation frequencies were found in tumors of the bile duct (cholangiocarcinomas, 35%), blood (T-cell acute lymphocytic leukemia, 31%), endometrium (9%), colon (9%), and stomach (6%). Approximately 43% of all mutations occur at two mutational "hotspots," which alter Arg residues (Arg465 and Arg479) that are critical for substrate recognition. Furthermore, we show that Fbxw7Arg465 hotspot mutant can abrogate wild-type Fbxw7 function through a dominant negative mechanism. Our study is the first comprehensive screen of FBXW7 mutations in various human malignancies and shows that FBXW7 is a general tumor suppressor in human cancer.
              Article 0 comments Cited 193 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Gang Zhang: zhanggangnjmu@126.com
                Shuwei Li: lisaqiu43@163.com
                Jiafei Lu: jiafeilu@foxmail.com
                Yuqiu Ge: yuqiuge0816@163.com
                Qiaoyan Wang: 112404317@qq.com
                Gaoxiang Ma: magaoxiang0805@sohu.com
                Qinghong Zhao: njzhqh@sina.com
                Dongdong Wu: ddw1011@163.com
                Weida Gong: gongweida@gmail.com
                Mulong Du: dumulong@163.com
                Haiyan Chu: chy_grape@126.com
                Meilin Wang: mwang@njmu.edu.cn
                Aihua Zhang: aihuagzykd@163.com
                Zhengdong Zhang: +86-25-8686-8423 , drzdzhang@gmail.com
                Journal
                Journal ID (nlm-ta): Mol Cancer
                Journal ID (iso-abbrev): Mol. Cancer
                Title: Molecular Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1476-4598
                Publication date (Electronic): 2 May 2018
                Publication date PMC-release: 2 May 2018
                Publication date Collection: 2018
                Volume: 17
                Electronic Location Identifier: 87
                Affiliations
                [1 ]GRID grid.452511.6, Department of Neurology, , Children’s Hospital of Nanjing Medical University, ; Nanjing, China
                [2 ]ISNI 0000 0000 9255 8984, GRID grid.89957.3a, Department of Environmental Genomics, School of Public Health, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, , Nanjing Medical University, ; 101 Longmian Avenue, Jiangning District, Nanjing, 211166 China
                [3 ]ISNI 0000 0000 9255 8984, GRID grid.89957.3a, Department of Genetic Toxicology, , The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, ; Nanjing, China
                [4 ]GRID grid.452511.6, Department of General Surgery, , The Second Affiliated Hospital of Nanjing Medical University, ; Nanjing, China
                [5 ]GRID grid.452931.8, Department of General Surgery, , Yixing Cancer Hospital, ; Yixing, China
                [6 ]ISNI 0000 0000 9330 9891, GRID grid.413458.f, Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, , Guizhou Medical University, ; Guiyang, 550025 Guizhou China
                Article
                Publisher ID: 829
                DOI: 10.1186/s12943-018-0829-6
                PMC ID: 5930724
                PubMed ID: 29720189
                SO-VID: 0d5e1400-c8a4-4baf-a496-7873cfad2d9a
                Copyright © © The Author(s). 2018
                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 : 13 August 2017
                Date accepted : 29 March 2018
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna,mt1jp,gastric cancer,cerna,prognosis
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna, mt1jp, gastric cancer, cerna, prognosis

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