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      TIPE1 suppresses invasion and migration through down‐regulating Wnt/β‐catenin pathway in gastric cancer

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          Abstract

          Epithelial–mesenchymal transition ( EMT) plays an important role in the invasiveness and metastasis of gastric cancer. Therefore, identifying key molecules involved in EMT will provide new therapeutic strategy for treating patients with gastric cancer. TIPE1 is a newly identified member of the TIPE ( TNFAIP8) family, and its contributions to progression and metastasis have not been evaluated. In this study, we found that the levels of TIPE1 were significantly reduced and inversely correlated with differentiation status and distant metastasis in primary gastric cancer tissues. We further observed overexpression of TIPE1 in aggressive gastric cancer cell lines decreased their metastatic properties both in vitro and in vivo as demonstrated by markedly inhibiting EMT and metastasis of gastric cancer cells in nude mice. Consistently, gene silencing of TIPE1 in well‐differentiated gastric cancer cell line ( AGS) inhibited these processes. Mechanistically, we found that TIPE1‐medicated Wnt/β‐catenin signalling was one of the critical signal transduction pathways that link TIPE1 to EMT inhibition. Importantly, TIPE1 dramatically restrained the expression and activities of MMP2 and MMP9 which are demonstrated to promote tumour progression and are implicated in EMT. Collectively, these findings provide new evidence for a better understanding of the biological activities of TIPE1 in progression and metastasis of gastric cancer and suggest that TIPE1 may be an innovative diagnostic and therapeutic target of gastric cancer.

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          Recent patterns in gastric cancer: a global overview.

          Paola Bertuccio, Liliane Chatenoud, Fabio Levi … (2009)
          Until the mid-1990s, gastric cancer has been the first cause of cancer death worldwide, although rates had been declining for several decades and gastric cancer has become a relatively rare cancer in North America and in most Northern and Western Europe, but not in Eastern Europe, Russia and selected areas of Central and South America or East Asia. We analyzed gastric cancer mortality in Europe and other areas of the world from 1980 to 2005 using joinpoint regression analysis, and provided updated site-specific incidence rates from 51 selected registries. Over the last decade, the annual percent change (APC) in mortality rate was around -3, -4% for the major European countries. The APC were similar for the Republic of Korea (APC = -4.3%), Australia (-3.7%), the USA (-3.6%), Japan (-3.5%), Ukraine (-3%) and the Russian Federation (-2.8%). In Latin America, the decline was less marked, but constant with APC around -1.6% in Chile and Brazil, -2.3% in Argentina and Mexico and -2.6% in Colombia. Cancers in the fundus and pylorus are more common in high incidence and mortality areas and have been declining more than cardia gastric cancer. Steady downward trends persist in gastric cancer mortality worldwide even in middle aged population, and hence further appreciable declines are likely in the near future.
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            Sonic hedgehog pathway promotes metastasis and lymphangiogenesis via activation of Akt, EMT, and MMP-9 pathway in gastric cancer.

            T. J. Kim, H. Kim, Peter M. Kang … (2011)
            Activation of sonic hedgehog (Shh) signaling has been implicated in progression of a variety of tumors. In this study, we elucidated a role for Shh in the invasion of gastric tumors and determined the mechanism by which Shh is regulated. Immunohistochemical analysis of 178 primary human gastric tumor biopsies indicated that Shh expression was positively correlated with lymph node metastasis, high lymphatic vessel density, and poor prognosis. In mouse xenograft models of human gastric cancer, enforced expression of Shh significantly enhanced the incidence of lung metastasis compared with nonexpressing controls. Mechanistic investigations revealed that phosphoinositide 3-kinase (PI3K)/Akt inhibition blocked Shh-induced epithelial-mesenchyme transition, the activity of matrix metalloproteinase 9 (MMP-9), and lymphangiogenesis, reducing tumor invasiveness and metastasis. Taken together, our findings establish that Shh signaling promotes the metastasis of gastric cancer through activation of the PI3K/Akt pathway, which leads to mesenchymal transition and MMP-9 activation. These findings offer preclinical validation of Shh as a candidate therapeutic target for treatment of metastatic gastric cancers. ©2011 AACR
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              Roles of Wnt/β-catenin signaling in the gastric cancer stem cells proliferation and salinomycin treatment

              J Mao, S Y S Fan, W. Ma … (2014)
              The Wnt1 protein, a secreted ligand that activates Wnt signaling pathways, contributes to the self-renewal of cancer stem cells (CSCs) and thus may be a major determinant of tumor progression and chemoresistance. In a series of gastric cancer specimens, we found strong correlations among Wnt1 expression, CD44 expression, and the grade of gastric cancer. Stable overexpression of Wnt1 increased AGS gastric cancer cells' proliferation rate and spheroids formation, which expressed CSC surface markers Oct4 and CD44. Subcutaneous injection of nude mice with Wnt1-overexpressing AGS cells resulted in larger tumors than injection of control AGS cells. Salinomycin, an antitumor agent, significantly reduced the volume of tumor caused by Wnt1-overexpressing AGS cells in vivo. This is achieved by inhibiting the proliferation of CD44+Oct4+ CSC subpopulation, at least partly through the suppression of Wnt1 and β-catenin expression. Taken together, activation of Wnt1 signaling accelerates the proliferation of gastric CSCs, whereas salinomycin acts to inhibit gastric tumor growth by suppressing Wnt signaling in CSCs. These results suggest that Wnt signaling might have a critical role in the self-renewal of gastric CSCs, and salinomycin targeting Wnt signaling may have important clinical applications in gastric cancer therapy.
              Article 0 comments Cited 110 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yan Zhang:
                ORCID: http://orcid.org/0000-0003-2219-5550
                zhangyan1978@sdu.edu.cn
                Fan Yi: fanyi@sdu.edu.cn
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 10 October 2017
                Publication date (Print): February 2018
                Volume: 22
                Issue: 2 ( doiID: 10.1111/jcmm.2018.22.issue-2 )
                Pages: 1103-1117
                Affiliations
                [ 1 ] Department of Pharmacology Shandong University School of Medicine Jinan China
                [ 2 ] Taishan District Center for Disease Control and Prevention Taian China
                [ 3 ] Department of Anesthesiology Qilu Hospital of Shandong University Jinan China
                [ 4 ] Department of Pediatrics Peoples Hospital of Rizhao Rizhao China
                [ 5 ] Department of Pathology Shandong University School of Medicine Jinan China
                [ 6 ] Department of Pathology Shandong Provincial Hospital Shandong University Jinan China
                [ 7 ] Key Laboratory of Cardiovascular Remodeling and Function Research Chinese Ministry of Education and Chinese Ministry of Health Qilu Hospital Shandong University Jinan China
                [ 8 ] Department of Immunology Shandong University School of Medicine Jinan China
                Author notes
                [*] [* ] Correspondence to: Fan YI

                E‐mail: fanyi@ 123456sdu.edu.cn

                Yan ZHANG

                E‐mail: zhangyan1978@ 123456sdu.edu.cn

                Author information
                http://orcid.org/0000-0003-2219-5550
                Article
                Publisher ID: JCMM13362
                DOI: 10.1111/jcmm.13362
                PMC ID: 5783849
                PubMed ID: 28994231
                SO-VID: 60171e8d-a079-49a1-9184-17333f4ee4e7
                Copyright © © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 07 June 2017
                Date accepted : 25 July 2017
                Page count
                Figures: 9, Tables: 1, Pages: 15, Words: 5561
                Funding
                Funded by: National Science Fund
                Award ID: 81525005
                Funded by: The National Nature Science Foundation of China
                Award ID: 81371317
                Award ID: 81328006
                Award ID: 81470958
                Award ID: 81470403
                Award ID: 81672093
                Award ID: 91642204
                Funded by: Key Research project of Shandong Province
                Award ID: 2016GGB14300
                Funded by: Key Research and Development Plan of Shandong Province
                Award ID: 2016GGE27013‐2016GSF201091
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id jcmm13362
                cover-date February 2018
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.3.1 mode:remove_FC converted:24.01.2018

                ScienceOpen disciplines: Molecular medicine
                Keywords: tipe1,gastric cancer,epithelial–mesenchymal transition,wnt/β‐catenin pathway
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: tipe1, gastric cancer, epithelial–mesenchymal transition, wnt/β‐catenin pathway

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