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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      Exosomal Tenascin-c induces proliferation and invasion of pancreatic cancer cells by WNT signaling

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive gastrointestinal malignancies. PDAC has an unfavorable prognosis and a 5-year survival rate of less than 6%. Early diagnosis is difficult and the disease progresses rapidly. Local invasion and distant metastases are the underlying reasons for PDAC patient death.

          Materials and Methods: By exosome proteomic analysis of homologous cell lines, we identified several proteins that distinguished highly- from less-invasive pancreatic cancer cells in situ. The third most prominent protein, Tenascin-c (TNC), was chosen to assess effects on the malignant characteristics of pancreatic cancer cells.

          Results: Silencing of TNC by short hairpin RNA (shRNA) in the cell lines PC-1.0 and Aspc-1 changed cellular proliferation, apoptosis, migration, and invasion. TNC expression was found to be positively related to proliferation and apoptosis, with each of these two processes reinforcing the other and regulated by the nuclear factor (NF)-κB pathway. TNC was found to promote PDAC cell line epithelial-mesenchymal transition by regulation of the Wnt/β-catenin pathway.

          Conclusions: This study demonstrated exosomal TNC to be closely associated with malignant features of pancreatic cancer cells including local invasion and distant metastasis. Hence, TNC is a potential therapeutic target for the treatment of PDAC invasiveness.

          Most cited references16

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          Microvesicles as mediators of intercellular communication in cancer--the emerging science of cellular 'debris'.

          Tae Lee, Esterina D'Asti, Nathalie Magnus … (2011)
          Cancer cells emit a heterogeneous mixture of vesicular, organelle-like structures (microvesicles, MVs) into their surroundings including blood and body fluids. MVs are generated via diverse biological mechanisms triggered by pathways involved in oncogenic transformation, microenvironmental stimulation, cellular activation, stress, or death. Vesiculation events occur either at the plasma membrane (ectosomes, shed vesicles) or within endosomal structures (exosomes). MVs are increasingly recognized as mediators of intercellular communication due to their capacity to merge with and transfer a repertoire of bioactive molecular content (cargo) to recipient cells. Such processes may occur both locally and systemically, contributing to the formation of microenvironmental fields and niches. The bioactive cargo of MVs may include growth factors and their receptors, proteases, adhesion molecules, signalling molecules, as well as DNA, mRNA, and microRNA (miRs) sequences. Tumour cells emit large quantities of MVs containing procoagulant, growth regulatory and oncogenic cargo (oncosomes), which can be transferred throughout the cancer cell population and to non-transformed stromal cells, endothelial cells and possibly to the inflammatory infiltrates (oncogenic field effect). These events likely impact tumour invasion, angiogenesis, metastasis, drug resistance, and cancer stem cell hierarchy. Ongoing studies explore the molecular mechanisms and mediators of MV-based intercellular communication (cancer vesiculome) with the hope of using this information as a possible source of therapeutic targets and disease biomarkers in cancer.
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            Tenascin-C at a glance.

            Kim S Midwood, Matthias Chiquet, Richard Tucker … (2016)
            Tenascin-C (TNC) is a hexameric, multimodular extracellular matrix protein with several molecular forms that are created through alternative splicing and protein modifications. It is highly conserved amongst vertebrates, and molecular phylogeny indicates that it evolved before fibronectin. Tenascin-C has many extracellular binding partners, including matrix components, soluble factors and pathogens; it also influences cell phenotype directly through interactions with cell surface receptors. Tenascin-C protein synthesis is tightly regulated, with widespread protein distribution in embryonic tissues, but restricted distribution of tenascin-C in adult tissues. Tenascin-C is also expressed de novo during wound healing or in pathological conditions, including chronic inflammation and cancer. First described as a modulator of cell adhesion, tenascin-C also directs a plethora of cell signaling and gene expression programs by shaping mechanical and biochemical cues within the cellular microenvironment. Exploitment of the pathological expression and function of tenascin-C is emerging as a promising strategy to develop new diagnostic, therapeutic and bioengineering tools. In this Cell Science at a Glance article and the accompanying poster we provide a succinct and comprehensive overview of the structural and functional features of tenascin-C and its potential roles in developing embryos and under pathological conditions.
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              Proteome profiling of exosomes derived from human primary and metastatic colorectal cancer cells reveal differential expression of key metastatic factors and signal transduction components.

              Christopher Adda, Alin Rai, Suresh Mathivanan … (2013)
              Exosomes are small extracellular 40-100 nm diameter membrane vesicles of late endosomal origin that can mediate intercellular transfer of RNAs and proteins to assist premetastatic niche formation. Using primary (SW480) and metastatic (SW620) human isogenic colorectal cancer cell lines we compared exosome protein profiles to yield valuable insights into metastatic factors and signaling molecules fundamental to tumor progression. Exosomes purified using OptiPrep™ density gradient fractionation were 40-100 nm in diameter, were of a buoyant density ~1.09 g/mL, and displayed stereotypic exosomal markers TSG101, Alix, and CD63. A major finding was the selective enrichment of metastatic factors (MET, S100A8, S100A9, TNC), signal transduction molecules (EFNB2, JAG1, SRC, TNIK), and lipid raft and lipid raft-associated components (CAV1, FLOT1, FLOT2, PROM1) in exosomes derived from metastatic SW620 cells. Additionally, using cryo-electron microscopy, ultrastructural components in exosomes were identified. A key finding of this study was the detection and colocalization of protein complexes EPCAM-CLDN7 and TNIK-RAP2A in colorectal cancer cell exosomes. The selective enrichment of metastatic factors and signaling pathway components in metastatic colon cancer cell-derived exosomes contributes to our understanding of the cross-talk between tumor and stromal cells in the tumor microenvironment. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OTT
                Journal ID (pmc): ott
                Title: OncoTargets and therapy
                Publisher: Dove
                ISSN (Electronic): 1178-6930
                Publication date (Electronic): 29 April 2019
                Publication date Collection: 2019
                Volume: 12
                Pages: 3197-3205
                Affiliations
                [1 ]First Department of General Surgery, Shengjing Hospital of China Medical University , Shenyang, Liaoning, People’s Republic of China
                Author notes
                Correspondence: Xiaodong TanFirst Department of General Surgery, Shengjing Hospital of China Medical University , No. 36 Sanhao Street, Heping District, Shenyang, Liaoning, People’s Republic of ChinaTel +860 249 6615Email tanxdcum@ 123456163.com
                Article
                Publisher ID: 192218
                DOI: 10.2147/OTT.S192218
                PMC ID: 6499136
                SO-VID: b34eddb7-081f-4fe6-b6d7-660129e85190
                Copyright © © 2019 Qian et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 25 October 2018
                Date accepted : 12 March 2019
                Page count
                Figures: 5, References: 22, Pages: 9
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: pancreatic ductal adenocarcinoma,tenascin-c,exosome,metastasis,wnt/β-catenin
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: pancreatic ductal adenocarcinoma, tenascin-c, exosome, metastasis, wnt/β-catenin

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