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      Human giant larvae-1 promotes migration and invasion of malignant glioma cells by regulating N-cadherin

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          Abstract

          Human giant larvae-1 (Hugl-1) is a human homologue of Drosophila tumor suppressor lethal ( 2)-giant larvae and has been reported to be involved in the development of human malignancies. Previous studies performed by our group demonstrated that Hugl-1 inhibits glioma cell proliferation in an intracranial model of nude mice. However, the exact molecular mechanisms underlying the participation of Hugl-1 in glioma invasion and migration, and in the depolarizing process remain largely unknown. Utilizing the U251-MG cells with stable expression of Hugl-1, the present study used wound healing, Transwell invasion and western blot assays to explore the role and specific mechanism of Hugl-1 in glioma invasion and migration. The results of the present study demonstrated that overexpression of Hugl-1 decreased cell-cell adhesion and increased cell-cell extracellular matrix adhesion. In addition, overexpression of Hugl-1 promoted pseudopodia formation, glioma cell migration and invasion. The molecular mechanism of action involved the negative regulation of N-cadherin protein levels by Hugl-1. Overexpression or knockdown of N-cadherin partially suppressed or enhanced the effects of Hugl-1 on glioma cell migration and invasion, respectively. Furthermore, Hugl-1 inhibited cell proliferation, while promoting cell migration, which suggests that it may serve a two-sided biological role in cellular processes. Taken together, these results suggest that Hugl-1 promotes the migration and invasion of malignant glioma cells by decreasing N-cadherin expression. Thus, Hugl-1 may be applied in the development of targeted and personalized treatment.

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          Most cited references 54

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          Cell adhesion and signalling by cadherins and Ig-CAMs in cancer.

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            Wnt signaling in cancer

            Wnt signaling is one of the key cascades regulating development and stemness, and has also been tightly associated with cancer. The role of Wnt signaling in carcinogenesis has most prominently been described for colorectal cancer, but aberrant Wnt signaling is observed in many more cancer entities. Here, we review current insights into novel components of Wnt pathways and describe their impact on cancer development. Furthermore, we highlight expanding functions of Wnt signaling for both solid and liquid tumors. We also describe current findings how Wnt signaling affects maintenance of cancer stem cells, metastasis and immune control. Finally, we provide an overview of current strategies to antagonize Wnt signaling in cancer and challenges that are associated with such approaches.
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              Tumor invasion in the absence of epithelial-mesenchymal transition: podoplanin-mediated remodeling of the actin cytoskeleton.

              The expression of podoplanin, a small mucin-like protein, is upregulated in the invasive front of a number of human carcinomas. We have investigated podoplanin function in cultured human breast cancer cells, in a mouse model of pancreatic beta cell carcinogenesis, and in human cancer biopsies. Our results indicate that podoplanin promotes tumor cell invasion in vitro and in vivo. Notably, the expression and subcellular localization of epithelial markers are unaltered, and mesenchymal markers are not induced in invasive podoplanin-expressing tumor cells. Rather, podoplanin induces collective cell migration by filopodia formation via the downregulation of the activities of small Rho family GTPases. In conclusion, podoplanin induces an alternative pathway of tumor cell invasion in the absence of epithelial-mesenchymal transition (EMT).
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                Author and article information

                Journal
                Oncol Lett
                Oncol Lett
                OL
                Oncology Letters
                D.A. Spandidos
                1792-1074
                1792-1082
                February 2021
                04 January 2021
                04 January 2021
                : 21
                : 2
                Affiliations
                [1 ]The Graduate School, Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China
                [2 ]Institute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China
                [3 ]Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China
                Author notes
                Correspondence to: Professor Xiuping Zhou, Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-hai Road, Xuzhou, Jiangsu 221002, P.R. China, E-mail: xpzhou@ 123456xzhmu.edu.cn
                Professor Rutong Yu, Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, 99 West Huai-hai Road, Xuzhou, Jiangsu 221002, P.R. China, E-mail: yu.rutong@ 123456163.com
                Article
                OL-0-0-12428
                10.3892/ol.2021.12428
                7798033
                Copyright: © Wang et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                Categories
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                Oncology & Radiotherapy

                n-cadherin, glioma, invasion, migration, hugl-1

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