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      FYN promotes gastric cancer metastasis by activating STAT3-mediated epithelial-mesenchymal transition

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          Abstract

          Gastric cancer is one of the most lethal cancers worldwide. FYN, a gene that is differentially expressed in gastric cancer, is considered a critical metastasis regulator in several solid tumors, but its role in gastric cancer is still unclear. This study aimed to evaluate the role of FYN and test whether FYN promotes migration and invasion of gastric cancer cells in vitro and in vivo via STAT3 signaling. FYN was overexpressed in gastric cancer and positively correlated with metastasis. FYN knockdown significantly decreased cancer cell migration and invasion, whereas FYN overexpression increased cancer migration and invasion. Genetic inhibition of FYN decreased the number of metastatic lung nodules in vivo. Several epithelial-mesenchymal transition markers were positively correlated with FYN expression, indicative of FYN involvement in this transition. Furthermore, gene set enrichment analysis of a Cancer Genome Atlas dataset revealed that the STAT3 signaling pathway was positively correlated with FYN expression. STAT3 inhibition reversed the FYN-mediated epithelial-mesenchymal transition and suppressed metastasis. In conclusion, FYN promotes gastric cancer metastasis possibly by activating STAT3-mediated epithelial mesenchymal transition and may be a novel therapeutic target for gastric cancer.

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          EMT Transition States during Tumor Progression and Metastasis

          Ievgenia Pastushenko, Cédric Blanpain (2018)
          Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells acquire mesenchymal features. In cancer, EMT is associated with tumor initiation, invasion, metastasis, and resistance to therapy. Recently, it has been demonstrated that EMT is not a binary process, but occurs through distinct cellular states. Here, we review the recent studies that demonstrate the existence of these different EMT states in cancer and the mechanisms regulating their functions. We discuss the different functional characteristics, such as proliferation, propagation, plasticity, invasion, and metastasis associated with the distinct EMT states. We summarize the role of the transcriptional and epigenetic landscapes, gene regulatory network and their surrounding niche in controlling the transition through the different EMT states.
          Article 0 comments Cited 953 times – based on 0 reviews     Review now
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            Novel roles of Src in cancer cell epithelial-to-mesenchymal transition, vascular permeability, microinvasion and metastasis.

            Ami Patel, Harika Sabbineni, Andrea Clarke … (2016)
            The Src-family kinases (SFKs), an intracellularly located group of non-receptor tyrosine kinases are involved in oncogenesis. The importance of SFKs has been implicated in the promotion of tumor cell motility, proliferation, inhibition of apoptosis, invasion and metastasis. Recent evidences indicate that specific effects of SFKs on epithelial-to-mesenchymal transition (EMT) as well as on endothelial and stromal cells in the tumor microenvironment can have profound effects on tumor microinvasion and metastasis. Although, having been studied extensively, these novel features of SFKs may contribute to greater understanding of benefits from Src inhibition in various types of cancers. Here we review the novel role of SFKs, particularly c-Src in mediating EMT, modulation of tumor endothelial-barrier, transendothelial migration (microinvasion) and metastasis of cancer cells, and discuss the utility of Src inhibitors in vascular normalization and cancer therapy.
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              No improvement in median survival for patients with metastatic gastric cancer despite increased use of chemotherapy.

              N. Bernards, G.J. Creemers, G.A.P. Nieuwenhuijzen … (2013)
              Gastric cancer often presents in a metastasized stage. We conducted a population-based study to evaluate trends in systemic treatment and survival of metastatic noncardia gastric cancer.
              Article 0 comments Cited 61 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                YuLong He
                ChangHua Zhang
                Journal
                Journal ID (nlm-ta): Transl Oncol
                Journal ID (iso-abbrev): Transl Oncol
                Title: Translational Oncology
                Publisher: Neoplasia Press
                ISSN (Electronic): 1936-5233
                Publication date PMC-release: 04 August 2020
                Publication date Collection: November 2020
                Publication date (Electronic): 04 August 2020
                Volume: 13
                Issue: 11
                Electronic Location Identifier: 100841
                Affiliations
                [a ]Department of Gastrointestinal Surgery, the First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan 2 nd Road, Guangzhou, Guangdong 510080, China
                [b ]Department of Gastrointestinal Surgery, the Seventh Affiliated Hospital of Sun Yat-sen University, 628 Zhenyuan Road, Shenzhen, Guangdong 518000, China
                Author notes
                [* ]Correspondence to: Y. He, Department of Gastrointestinal Surgery, The First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan 2nd Road, Guangzhou, Guangdong 510080, China. heyulong@ 123456mail.sysu.edu.cn
                [** ]Corresponding author. zhchangh@ 123456mail.sysu.edu.cn
                [1]

                These authors contributed equally to this work.

                Article
                Publisher ID: S1936-5233(20)30333-8 Publisher ID: 100841
                DOI: 10.1016/j.tranon.2020.100841
                PMC ID: 7408597
                PubMed ID: 32763503
                SO-VID: 7088ef58-855e-4e2d-a33f-4445b826b741
                Copyright © © 2020 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 28 May 2020
                Date revision received : 1 July 2020
                Date accepted : 19 July 2020
                Categories
                Subject: Original article

                Keywords: fyn,cell migration,cell invasion,therapeutic target,gc, gastric cancer,gsea, gene set enrichment analysis,sirna, small interference rna,os, overall survival,dfs, disease free survival,emt, epithelial mesenchymal transition,sfks, src family of protein tyrosine kinases
                Data availability:
                Keywords: fyn, cell migration, cell invasion, therapeutic target, gc, gastric cancer, gsea, gene set enrichment analysis, sirna, small interference rna, os, overall survival, dfs, disease free survival, emt, epithelial mesenchymal transition, sfks, src family of protein tyrosine kinases

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