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      CD146, from a melanoma cell adhesion molecule to a signaling receptor

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          Abstract

          CD146 was originally identified as a melanoma cell adhesion molecule (MCAM) and highly expressed in many tumors and endothelial cells. However, the evidence that CD146 acts as an adhesion molecule to mediate a homophilic adhesion through the direct interactions between CD146 and itself is still lacking. Recent evidence revealed that CD146 is not merely an adhesion molecule, but also a cellular surface receptor of miscellaneous ligands, including some growth factors and extracellular matrixes. Through the bidirectional interactions with its ligands, CD146 is actively involved in numerous physiological and pathological processes of cells. Overexpression of CD146 can be observed in most of malignancies and is implicated in nearly every step of the development and progression of cancers, especially vascular and lymphatic metastasis. Thus, immunotherapy against CD146 would provide a promising strategy to inhibit metastasis, which accounts for the majority of cancer-associated deaths. Therefore, to deepen the understanding of CD146, we review the reports describing the newly identified ligands of CD146 and discuss the implications of these findings in establishing novel strategies for cancer therapy.

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          Pericyte loss and microaneurysm formation in PDGF-B-deficient mice.

          Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.
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            The MAPK signaling cascade.

            The transmission of extracellular signals into their intracellular targets is mediated by a network of interacting proteins that regulate a large number of cellular processes. Cumulative efforts from many laboratories over the past decade have allowed the elucidation of one such signaling mechanism, which involves activations of several membranal signaling molecules followed by a sequential stimulation of several cytoplasmic protein kinases collectively known as mitogen-activated protein kinase (MAPK) signaling cascade. Up to six tiers in this cascade contribute to the amplification and specificity of the transmitted signals that eventually activate several regulatory molecules in the cytoplasm and in the nucleus to initiate cellular processes such as proliferation, differentiation, and development. Moreover, because many oncogenes have been shown to encode proteins that transmit mitogenic signals upstream of this cascade, the MAPK pathway provides a simple unifying explanation for the mechanism of action of most, if not all, nonnuclear oncogenes. The pattern of MAPK cascade is not restricted to growth factor signaling and it is now known that signaling pathways initiated by phorbol esters, ionophors, heat shock, and ligands for seven transmembrane receptors use distinct MAPK cascades with little or no cross-reactivity between them. In this review we emphasize primarily the first MAPK cascade to be discovered that uses the MEK and ERK isoforms and describe their involvement in different cellular processes.
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              Galectins as modulators of tumour progression.

              Galectins are a family of animal lectins with diverse biological activities. They function both extracellularly, by interacting with cell-surface and extracellular matrix glycoproteins and glycolipids, and intracellularly, by interacting with cytoplasmic and nuclear proteins to modulate signalling pathways. Current research indicates that galectins have important roles in cancer; they contribute to neoplastic transformation, tumour cell survival, angiogenesis and tumour metastasis. They can modulate the immune and inflammatory responses and might have a key role helping tumours to escape immune surveillance. How do the different members of the Galectin family contribute to these diverse aspects of tumour biology?
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                Author and article information

                Contributors
                clairezqwang@hotmail.com
                yanxy@ibp.ac.cn
                Journal
                Signal Transduct Target Ther
                Signal Transduct Target Ther
                Signal Transduction and Targeted Therapy
                Nature Publishing Group UK (London )
                2095-9907
                2059-3635
                11 August 2020
                11 August 2020
                2020
                : 5
                : 148
                Affiliations
                [1 ]GRID grid.9227.e, ISNI 0000000119573309, Key Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, , Chinese Academy of Sciences, ; 100101 Beijing, China
                [2 ]GRID grid.410726.6, ISNI 0000 0004 1797 8419, College of Life Science, , University of Chinese Academy of Sciences, ; 100049 Beijing, China
                [3 ]GRID grid.24696.3f, ISNI 0000 0004 0369 153X, Department of Gastrointestinal Hepatobiliary Tumor Surgery, Beijing Shijitan Hospital, , Capital Medical University, ; 100038 Beijing, China
                [4 ]GRID grid.24696.3f, ISNI 0000 0004 0369 153X, Departments of Pathology, Beijing Shijitan Hospital, , Capital Medical University, ; 100038 Beijing, China
                [5 ]GRID grid.207374.5, ISNI 0000 0001 2189 3846, Nanozyme Medical Center, School of Basic Medical Sciences, , Zhengzhou University, ; Zhengzhou, 450001 China
                Article
                259
                10.1038/s41392-020-00259-8
                7421905
                32782280
                913a4154-6304-40b7-81da-a2a5132ab3b1
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 21 March 2020
                : 14 June 2020
                : 18 June 2020
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100002855, Ministry of Science and Technology of the People’s Republic of China (Chinese Ministry of Science and Technology);
                Award ID: 2018ZX10101004002004
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/501100004826, Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation);
                Award ID: 7192123
                Award Recipient :
                Funded by: The first grant is the National Key Technology Research and Development Program of the Ministry of Science and Technology of China(No.2018ZX10101004002004)
                Categories
                Review Article
                Custom metadata
                © The Author(s) 2020

                cell biology,tumour angiogenesis
                cell biology, tumour angiogenesis

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