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      CD146 promotes migration and proliferation in pulmonary large cell neuroendocrine carcinoma cell lines

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          Abstract

          Dysregulated expression of the cell surface protein, CD146, has been implicated in various types of cancer in humans, including in lung cancer. The present study aimed to clarify the mechanism underlying abnormal CD146 expression in human pulmonary large cell neuroendocrine carcinoma (LCNEC) cell lines (NCI-H460 and NCI-H810). The functions of CD146 were investigated by measuring cell migration and viability following CD146 knockdown or overexpression via small interference RNA and plasmid transfection. The findings demonstrated that decreased protein expression of CD146 could inhibit migration and viability in LCNEC cells. Furthermore, CD146 was determined to influence the expression of epithelial-mesenchymal transition markers (epithelial cadherin, vimentin and Snail) and promoted AKT phosphorylation. The present results imply CD146 may function in the migration and proliferation of pulmonary LCNEC cells.

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          CD146, a multi-functional molecule beyond adhesion.

          ZHAOQING WANG, Xiyun Yan (2013)
          CD146 is a cell adhesion molecule (CAM) that is primarily expressed at the intercellular junction of endothelial cells. CD146 was originally identified as a tumor marker for melanoma (MCAM) due to its existence only in melanoma but not in the corresponding normal counterpart. However CD146 is not just a CAM for the inter-cellular and cell-matrix adhesion. Recent evidence indicates that CD146 is actively involved in miscellaneous processes, such as development, signaling transduction, cell migration, mesenchymal stem cells differentiation, angiogenesis and immune response. CD146 has increasingly become an important molecule, especially identified as a novel bio-marker for angiogenesis and for cancer. Here we have reviewed the dynamic research of CD146, particularly newly identified functions and the underlying mechanisms of CD146. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
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            Genomic Profiling of Large-Cell Neuroendocrine Carcinoma of the Lung.

            Tomohiro Miyoshi, Shigeki Umemura, Yuki Matsumura … (2017)
            Although large-cell neuroendocrine carcinoma (LCNEC) of the lung shares many clinical characteristics with small-cell lung cancer (SCLC), little is known about its molecular features. We analyzed lung LCNECs to identify biologically relevant genomic alterations.
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              CD146, an epithelial-mesenchymal transition inducer, is associated with triple-negative breast cancer.

              Qiqun Zeng, Weidong Li, Di Lu … (2012)
              The epithelial-mesenchymal transition (EMT) plays an important role in breast cancer metastasis, especially in the most aggressive and lethal subtype, "triple-negative breast cancer" (TNBC). Here, we report that CD146 is a unique activator of EMTs and significantly correlates with TNBC. In epithelial breast cancer cells, overexpression of CD146 down-regulated epithelial markers and up-regulated mesenchymal markers, significantly promoted cell migration and invasion, and induced cancer stem cell-like properties. We further found that RhoA pathways positively regulated CD146-induced EMTs via the key EMT transcriptional factor Slug. An orthotopic breast tumor model demonstrated that CD146-overexpressing breast tumors showed a poorly differentiated phenotype and displayed increased tumor invasion and metastasis. We confirmed these findings by conducting an immunohistochemical analysis of 505 human primary breast tumor tissues and found that CD146 expression was significantly associated with high tumor stage, poor prognosis, and TNBC. CD146 was expressed at abnormally high levels (68.9%), and was strongly associated with E-cadherin down-regulation in TNBC samples. Taken together, these findings provide unique evidence that CD146 promotes breast cancer progression by induction of EMTs via the activation of RhoA and up-regulation of Slug. Thus, CD146 could be a therapeutic target for breast cancer, especially for TNBC.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Lett
                Journal ID (iso-abbrev): Oncol Lett
                Journal ID (publisher-id): OL
                Title: Oncology Letters
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-1074
                ISSN (Electronic): 1792-1082
                Publication date (Print): February 2019
                Publication date (Electronic): 14 December 2018
                Publication date PMC-release: 14 December 2018
                Volume: 17
                Issue: 2
                Pages: 2075-2080
                Affiliations
                [1 ]Department of Critical Care Medicine, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital and Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong 518116, P.R. China
                [2 ]Department of Medical Administration, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China
                [3 ]Department of General Surgery, Harbin Children Hospital, Harbin, Heilongjiang 150001, P.R. China
                [4 ]Department of Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital and Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, Guangdong 518116, P.R. China
                [5 ]Department of Critical Care Medicine, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, P.R. China
                Author notes
                Correspondence to: Dr Biao Zheng, Department of Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital and Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 113 Baohe Road, Shenzhen, Guangdong 518116, P.R. China, E-mail: jeongpyo@ 123456live.com
                Dr Yong Gao, Department of Critical Care Medicine, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 17 Panjiayuan Nanli, Beijing 100021, P.R. China, E-mail: 13801089949@ 123456163.com
                [*]

                Contributed equally

                Article
                Publisher ID: OL-0-0-9830
                DOI: 10.3892/ol.2018.9830
                PMC ID: 6341587
                PubMed ID: 30675274
                SO-VID: c5bcbc80-2e23-4704-af86-6ab5c376dd28
                Copyright © Copyright: © Piao et al.
                License:

                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.

                History
                Date received : 21 December 2017
                Date accepted : 06 September 2018
                Categories
                Subject: Articles

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cluster of differentiation 146,pulmonary large cell neuroendocrine carcinoma,epithelial-mesenchymal transition,akt
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cluster of differentiation 146, pulmonary large cell neuroendocrine carcinoma, epithelial-mesenchymal transition, akt

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