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      Regulation and functions of integrin α2 in cell adhesion and disease


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          Integrins are cell adhesion molecules that are composed of an alpha (α) subunit and a beta (β) subunit with affinity for different extracellular membrane components. The integrin family includes 24 known members that actively regulate cellular growth, differentiation, and apoptosis. Each integrin heterodimer has a particular function in defined contexts as well as some partially overlapping features with other members in the family. As many reviews have covered the general integrin family in molecular and cellular studies in life science, this review will focus on the specific regulation, function, and signaling of integrin α2 subunit (CD49b, VLA-2; encoded by the gene ITGA2) in partnership with β1 (CD29) subunit in normal and cancer cells. Its roles in cell adhesion, cell motility, angiogenesis, stemness, and immune/blood cell regulations are discussed. The pivotal role of integrin α2 in many diseases such as cancer suggests its potential to be used as a novel therapeutic target.

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          Keeping abreast of the mammary epithelial hierarchy and breast tumorigenesis.

          The epithelium of the mammary gland exists in a highly dynamic state, undergoing dramatic morphogenetic changes during puberty, pregnancy, lactation, and regression. The recent identification of stem and progenitor populations in mouse and human mammary tissue has provided evidence that the mammary epithelium is organized in a hierarchical manner. Characterization of these normal epithelial subtypes is an important step toward understanding which cells are predisposed to oncogenesis. This review summarizes progress in the field toward defining constituent cells and key molecular regulators of the mammary epithelial hierarchy. Potential relationships between normal epithelial populations and breast tumor subtypes are discussed, with implications for understanding the cellular etiology underpinning breast tumor heterogeneity.
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            With the goal to remove the roots of cancer, eliminate metastatic seeds, and overcome therapy resistance, the 2014 inaugural International Cancer Stem Cell (CSC) Conference at Cleveland, OH, convened together over 320 investigators, including 55 invited world-class speakers, 25 short oral presenters, and 100 poster presenters, to gain an in-depth understanding of CSCs and explore therapeutic opportunities targeting CSCs. The meeting enabled intriguing discussions on several topics including: genetics and epigenetics; cancer origin and evolution; microenvironment and exosomes; metabolism and inflammation; metastasis and therapy resistance; single cell and heterogeneity; plasticity and reprogramming; as well as other new concepts. Reports of clinical trials targeting CSCs emphasized the urgent need for strategically designing combinational CSC-targeting therapies against cancer.
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              Integrin activation.

              The ability of cells to regulate dynamically their adhesion to one another and to the extracellular matrix (ECM) that surrounds them is essential in multicellular organisms. The integrin family of transmembrane adhesion receptors mediates both cell-cell and cell-ECM adhesion. One important, rapid and reversible mechanism for regulating adhesion is by increasing the affinity of integrin receptors for their extracellular ligands (integrin activation). This is controlled by intracellular signals that, through their action on integrin cytoplasmic domains, induce conformational changes in integrin extracellular domains that result in increased affinity for ligand. Recent studies have shed light on the final intracellular steps in this process and have revealed a vital role for the cytoskeletal protein talin.

                Author and article information

                Genes Dis
                Genes Dis
                Genes & Diseases
                Chongqing Medical University
                31 December 2018
                March 2019
                31 December 2018
                : 6
                : 1
                : 16-24
                [a ]Department of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
                [b ]Department of Pharmacology Graduate Program, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
                [c ]Department of Medicine, Hematology/Oncology Division, Northwestern University, Chicago, IL 60611, USA
                [d ]Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
                [e ]Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
                Author notes
                []Corresponding author. Northwestern University, Chicago, IL 60611, USA. huiping.liu@ 123456northwestern.edu
                [∗∗ ]Corresponding author. Northwestern University, Chicago, IL 60611, USA. valery.adorno-cruz@ 123456northwestern.edu
                © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                : 21 September 2018
                : 24 December 2018

                integrin α2,cd49b,molecular mechanisms,regulation,signaling


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