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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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          Most cited references 58

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          Convergence of Wnt, beta-catenin, and cadherin pathways.

           W Nelson,  Ferric Fang (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.

            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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              Inflammation and EMT: an alliance towards organ fibrosis and cancer progression

              Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases. The EMT is a crucial process in the development of different tissues in the embryo and its reactivation in the adult may be regarded as a physiological attempt to control inflammatory responses and to ‘heal’ damaged tissue. However, in pathological contexts such as in tumours or during the development of organ fibrosis, this healing response adopts a sinister nature, steering these diseases towards metastasis and organ failure. Importantly, the chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.
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                Author and article information

                Contributors
                Journal
                Front Oncol
                Front Oncol
                Front. Oncol.
                Frontiers in Oncology
                Frontiers Media S.A.
                2234-943X
                25 January 2019
                2019
                : 9
                Affiliations
                1Department of Anesthesiology, Dalian Medical University , Dalian, China
                2Department of Anesthesiology, First Affiliated Hospital of Dalian Medical University , Dalian, China
                3Department of Anesthesia and Intensive Care, School of Medicine and Health Science, University for Development Studies , Tamale, Ghana
                4Department of Biochemistry and Molecular Biology, Dalian Medical University , Dalian, China
                5Department of Biotechnology, Dalian Medical University , Dalian, China
                6Department of Radiology, Dalian Medical University , Dalian, China
                7Department of Clinical Microbiology, School of Medicine and Health Science, University for Development Studies , Tamale, Ghana
                8School of Life Science and Bio-pharmaceutics, Shenyang Pharmaceutical University , Shenyang, China
                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
                10.3389/fonc.2019.00021
                6355678
                Copyright © 2019 Kampo, Ahmmed, Zhou, Owusu, Anabah, Doudou, Kuugbee, Cui, Lu, Yan and Wen.

                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.

                Page count
                Figures: 7, Tables: 0, Equations: 1, References: 78, Pages: 17, Words: 11484
                Categories
                Oncology
                Original Research

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