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      Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

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          Abstract

          A scorpion peptide reported to exhibit both analgesic and antitumor activity in animal models may present as an alternative therapeutic agent for breast cancer. We aimed to investigate the effect of Buthus martensii Karsch antitumor-analgesic peptide (BmK AGAP) on breast cancer cell stemness and epithelial-mesenchymal transition (EMT). We treated MCF-7 and MDA-MB-231 cells with different concentrations of rBmK AGAP and observed that rBmK AGAP inhibited cancer cell stemness, epithelial-mesenchymal transition (EMT), migration, and invasion. Analysis by qPCR, ELISA, western blot, immunofluorescence staining, sphere formation, colony assay, transwell migration, and invasion assays demonstrated rBmK AGAP treatment decreased the expressions of Oct4, Sox2, N-cadherin, Snail, and increased the expression of E-cadherin. rBmK AGAP inhibited breast cancer cell stemness, EMT, migration, and invasion by down-regulating PTX3 through NF-κB and Wnt/β-catenin signaling Pathway in vitro and in vivo. Xenograft tumor model confirmed inhibition of tumor growth, stem-like features, and EMT by rBmK AGAP. Thus, rBmK AGAP is a potential therapeutic agent against breast cancer and related pain.

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          Origin and physiological roles of inflammation.

          Ruslan Medzhitov (2008)
          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Convergence of Wnt, beta-catenin, and cadherin pathways.

            W Nelson (2004)
            The specification and proper arrangements of new cell types during tissue differentiation require the coordinated regulation of gene expression and precise interactions between neighboring cells. Of the many growth factors involved in these events, Wnts are particularly interesting regulators, because a key component of their signaling pathway, beta-catenin, also functions as a component of the cadherin complex, which controls cell-cell adhesion and influences cell migration. Here, we assemble evidence of possible interrelations between Wnt and other growth factor signaling, beta-catenin functions, and cadherin-mediated adhesion.
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              Opinion: migrating cancer stem cells - an integrated concept of malignant tumour progression.

              Thomas Brabletz, Andreas Jung, Simone Spaderna … (2005)
              The dissemination of tumour cells is the prerequisite of metastases and is correlated with a loss of epithelial differentiation and the acquisition of a migratory phenotype, a hallmark of malignant tumour progression. A stepwise, irreversible accumulation of genetic alterations is considered to be the responsible driving force. But strikingly, metastases of most carcinomas recapitulate the organization of their primary tumours. Although current models explain distinct and important aspects of carcinogenesis, each alone can not explain the sum of the cellular changes apparent in human cancer progression. We suggest an extended, integrated model that is consistent with all aspects of human tumour progression - the 'migrating cancer stem (MCS)-cell' concept.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Oncol
                Journal ID (iso-abbrev): Front Oncol
                Journal ID (publisher-id): Front. Oncol.
                Title: Frontiers in Oncology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 2234-943X
                Publication date (Electronic): 25 January 2019
                Publication date Collection: 2019
                Volume: 9
                Electronic Location Identifier: 21
                Affiliations
                [1] 1Department of Anesthesiology, Dalian Medical University , Dalian, China
                [2] 2Department of Anesthesiology, First Affiliated Hospital of Dalian Medical University , Dalian, China
                [3] 3Department of Anesthesia and Intensive Care, School of Medicine and Health Science, University for Development Studies , Tamale, Ghana
                [4] 4Department of Biochemistry and Molecular Biology, Dalian Medical University , Dalian, China
                [5] 5Department of Biotechnology, Dalian Medical University , Dalian, China
                [6] 6Department of Radiology, Dalian Medical University , Dalian, China
                [7] 7Department of Clinical Microbiology, School of Medicine and Health Science, University for Development Studies , Tamale, Ghana
                [8] 8School of Life Science and Bio-pharmaceutics, Shenyang Pharmaceutical University , Shenyang, China
                [9] 9Department of Ophthalmology, First Affiliated Hospital of Dalian Medical University , Dalian, China
                Author notes

                Edited by: Emily Catherine Bellavance, University of Maryland, Baltimore, United States

                Reviewed by: Saori Furuta, University of Toledo, United States; Lianjin Jin, Tulane University, United States

                *Correspondence: Qing-Ping Wen wqp.89@ 123456163.com

                This article was submitted to Women's Cancer, a section of the journal Frontiers in Oncology

                Article
                DOI: 10.3389/fonc.2019.00021
                PMC ID: 6355678
                PubMed ID: 30740360
                SO-VID: 8d5383b9-0a89-4f4d-99c5-8605d57e5b0e
                Copyright © Copyright © 2019 Kampo, Ahmmed, Zhou, Owusu, Anabah, Doudou, Kuugbee, Cui, Lu, Yan and Wen.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 21 August 2018
                Date accepted : 07 January 2019
                Page count
                Figures: 7, Tables: 0, Equations: 1, References: 78, Pages: 17, Words: 11484
                Categories
                Subject: Oncology
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: scorpion venom analgesic peptide,rbmk agap,stemness,epithelial-mesenchymal transition,pentraxin 3,wnt/β-catenin signaling,transcription factor nf-κb,breast cancer
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: scorpion venom analgesic peptide, rbmk agap, stemness, epithelial-mesenchymal transition, pentraxin 3, wnt/β-catenin signaling, transcription factor nf-κb, breast cancer

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