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Cell Adhesion Signaling and Its Impact on Tumorigenesis

Cell Adhesion Signaling and Its Impact on Tumorigenesis Hindawi Publishing Corporation Journal of Oncology Volume 2010, Article ID 257809, 2 pages doi:10.1155/2010/257809 Editorial 1 2, 3 4 Claudia D. Andl, Ala-Eddin Al Moustafa, Therese B. Deramaudt, 5, 6 and Geraldine M. O’Neill Vanderbilt University, Nashville, TN, USA Syrian Research Cancer Centre of the Syrian Society against Cancer, Aleppo, Syria McGill & Concordia Universities, Montreal, Canada Universite de Strasbourg, CNRS UMR 7213, Illkirch, France Kids Research Institute, The Children’s Hospital at Westmead, Sydney, NSW 2145, Australia Discipline of Paediatrics and Child Health, The University of Sydney, Sydney, NSW 2006, Australia Correspondence should be addressed to Claudia D. Andl, claudia.andl@vanderbilt.edu Received 20 December 2010; Accepted 20 December 2010 Copyright © 2010 Claudia D. Andl et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cell adhesion can be divided into cell-cell adhesion medi- however, little is known regarding the mechanisms behind ated by three major structures, tight junctions, adherens their pathophysiological function. Drs. Singh, Sharma, and junctions, desmosomes, and cell-matrix adhesion, which Dhawan give an overview of the current state of knowledge is for the most part integrin-based. Cell-cell interactions in this issue. To identify cell transformation mechanisms play an important role in the maintenance and integrity other than previously described, Lynch et al. investigated of tissues and organs but similar to cell-matrix complexes the effect of MMP-7 mediated cleavage of E-cadherin. may also transduce cell signaling. While this is the basics for They demonstrate that loss of cell-cell adhesion is induced understanding cell adhesion and its function, the role of cell following E-cadherin processing, which results in increased adhesion proteins in disease, especially tumorigenesis, is far cell migration, loss of polarization, and activation of RhoA. more diverse. A summary is given in the paper presented Interactions of cell adhesion molecules with their envi- by Dr. Andl in this issue where she also focuses on recently ronment are central to their regulation and to cell migration discovered cell adhesion components and the regulation of and invasion. In the tumor context, the array of integrin cell adhesion molecules by miRNAs. In cancer, cell adhesion receptors expressed causes the cells to differentially respond molecules are generally thought to be deactivated in order to external signals, resist the effects of cytotoxic drugs, and to aid in cancer cell dissemination and dispersal. However, facilitate growth and invasion through a range of different aside from the loss of function, various gain-of-function tissue environments encountered by invasive cancer cells. events occur during induction and progression of cancer In particular, the regulation of integrin receptor interaction that can be mediated by cell adhesion molecules. Many with the extracellular matrix is thought to be critical for those of the molecules involved in these processes, such as the cancers that invade and metastasize using a mesenchymal components of desmosomes, were initially identified as mode of migration. Jossen et al. show a novel prostate targets of autoimmune diseases. This special issue outlines cancer bone metastatic model to assay drug sensitivity in the latest findings in research and review articles. three-dimensional cultures that mimic the preclinical or Tight junctions mediate apical cell-cell adhesion and clinical setting more accurately. In here, they show that regulate epithelial cell polarity. Members of the claudin prostate cells revert to more epithelial cells, mesenchymal- family are involved in a number of diseases including cancer; epithelial transition (MET) in the presence of bone stroma 2 Journal of Oncology modeling later stages of metastatic colonization, and are sensitized to radiation treatment when blocking E-cadherin or α-integrin. Mesenchymal migration as a therapeutic target for glioblastoma is discussed by Zhong et al. Another potential therapeutic agent, a Src inhibitor, is described by Yaseem et al. Comparison of SKI-606 and Iressa effects, Src/Abl and EGFR inhibitors, respectively, on cervical cancer cell lines shows inhibition of cell proliferation. Additionally, SKI-606 decreases cell migration and invasion through MET accompanied by the re-expression of E-cadherin and the recruitment of β-catenin to the cell membrane. Hironobu Yamashita et al. demonstrate that lysophosphatidic acid, a phospholipid growth factor, induces the stimulation of lamellipodia formation and enhanced cell migration through the upregulation of the TGFβ1 target gene Laminin-322. The role of focal adhesion kinase (FAK) phosphorylation in the dynamic regulation of integrin-based adhesions and cellular migration is shown in a paper by Hamadi et al. Upon pervanadate-induced phosphorylation, FAK delocal- izes from focal adhesions to newly formed membrane ruffles in a src-dependent event. Finally, advances in nanotech- nology that allow the study of cellular transformation in engineered cellular environments are introduced by Siti Hawa Ngalmi et al. Such cross-disciplinary approaches have begun to advance our knowledge of how adhesion signaling is organized and how cells relay information regarding the composition and structure of the external environment into biological activity. In particular, these advances are being driven by novel microscopy technologies and the continuing development of new techniques that allow us to visualize the intricate workings of adhesion-dependent signaling processes. This synopsis gives a glimpse at the current leading edge science published in this special issue of the Journal of Oncology. We hope that these papers inspire interest in multidisciplinary approaches as well as in the identification of novel therapeutics. Claudia D. Andl Ala-Eddin Al Moustafa Therese B. Deramaudt Geraldine M. O’Neill MEDIATORS of INFLAMMATION The Scientific Gastroenterology Journal of World Journal Research and Practice Diabetes Research Disease Markers Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 International Journal of Journal of Immunology Research Endocrinology Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Submit your manuscripts at http://www.hindawi.com BioMed PPAR Research Research International Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Journal of Obesity Evidence-Based Journal of Journal of Stem Cells Complementary and Ophthalmology International Alternative Medicine Oncology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Parkinson’s Disease Computational and Behavioural Mathematical Methods AIDS Oxidative Medicine and in Medicine Research and Treatment Cellular Longevity Neurology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Oncology Hindawi Publishing Corporation

Cell Adhesion Signaling and Its Impact on Tumorigenesis

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Publisher
Hindawi Publishing Corporation
Copyright
Copyright © 2010 Claudia D. Andl et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ISSN
1687-8450
eISSN
1687-8469
DOI
10.1155/2010/257809
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Abstract

Hindawi Publishing Corporation Journal of Oncology Volume 2010, Article ID 257809, 2 pages doi:10.1155/2010/257809 Editorial 1 2, 3 4 Claudia D. Andl, Ala-Eddin Al Moustafa, Therese B. Deramaudt, 5, 6 and Geraldine M. O’Neill Vanderbilt University, Nashville, TN, USA Syrian Research Cancer Centre of the Syrian Society against Cancer, Aleppo, Syria McGill & Concordia Universities, Montreal, Canada Universite de Strasbourg, CNRS UMR 7213, Illkirch, France Kids Research Institute, The Children’s Hospital at Westmead, Sydney, NSW 2145, Australia Discipline of Paediatrics and Child Health, The University of Sydney, Sydney, NSW 2006, Australia Correspondence should be addressed to Claudia D. Andl, claudia.andl@vanderbilt.edu Received 20 December 2010; Accepted 20 December 2010 Copyright © 2010 Claudia D. Andl et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cell adhesion can be divided into cell-cell adhesion medi- however, little is known regarding the mechanisms behind ated by three major structures, tight junctions, adherens their pathophysiological function. Drs. Singh, Sharma, and junctions, desmosomes, and cell-matrix adhesion, which Dhawan give an overview of the current state of knowledge is for the most part integrin-based. Cell-cell interactions in this issue. To identify cell transformation mechanisms play an important role in the maintenance and integrity other than previously described, Lynch et al. investigated of tissues and organs but similar to cell-matrix complexes the effect of MMP-7 mediated cleavage of E-cadherin. may also transduce cell signaling. While this is the basics for They demonstrate that loss of cell-cell adhesion is induced understanding cell adhesion and its function, the role of cell following E-cadherin processing, which results in increased adhesion proteins in disease, especially tumorigenesis, is far cell migration, loss of polarization, and activation of RhoA. more diverse. A summary is given in the paper presented Interactions of cell adhesion molecules with their envi- by Dr. Andl in this issue where she also focuses on recently ronment are central to their regulation and to cell migration discovered cell adhesion components and the regulation of and invasion. In the tumor context, the array of integrin cell adhesion molecules by miRNAs. In cancer, cell adhesion receptors expressed causes the cells to differentially respond molecules are generally thought to be deactivated in order to external signals, resist the effects of cytotoxic drugs, and to aid in cancer cell dissemination and dispersal. However, facilitate growth and invasion through a range of different aside from the loss of function, various gain-of-function tissue environments encountered by invasive cancer cells. events occur during induction and progression of cancer In particular, the regulation of integrin receptor interaction that can be mediated by cell adhesion molecules. Many with the extracellular matrix is thought to be critical for those of the molecules involved in these processes, such as the cancers that invade and metastasize using a mesenchymal components of desmosomes, were initially identified as mode of migration. Jossen et al. show a novel prostate targets of autoimmune diseases. This special issue outlines cancer bone metastatic model to assay drug sensitivity in the latest findings in research and review articles. three-dimensional cultures that mimic the preclinical or Tight junctions mediate apical cell-cell adhesion and clinical setting more accurately. In here, they show that regulate epithelial cell polarity. Members of the claudin prostate cells revert to more epithelial cells, mesenchymal- family are involved in a number of diseases including cancer; epithelial transition (MET) in the presence of bone stroma 2 Journal of Oncology modeling later stages of metastatic colonization, and are sensitized to radiation treatment when blocking E-cadherin or α-integrin. Mesenchymal migration as a therapeutic target for glioblastoma is discussed by Zhong et al. Another potential therapeutic agent, a Src inhibitor, is described by Yaseem et al. Comparison of SKI-606 and Iressa effects, Src/Abl and EGFR inhibitors, respectively, on cervical cancer cell lines shows inhibition of cell proliferation. Additionally, SKI-606 decreases cell migration and invasion through MET accompanied by the re-expression of E-cadherin and the recruitment of β-catenin to the cell membrane. Hironobu Yamashita et al. demonstrate that lysophosphatidic acid, a phospholipid growth factor, induces the stimulation of lamellipodia formation and enhanced cell migration through the upregulation of the TGFβ1 target gene Laminin-322. The role of focal adhesion kinase (FAK) phosphorylation in the dynamic regulation of integrin-based adhesions and cellular migration is shown in a paper by Hamadi et al. Upon pervanadate-induced phosphorylation, FAK delocal- izes from focal adhesions to newly formed membrane ruffles in a src-dependent event. Finally, advances in nanotech- nology that allow the study of cellular transformation in engineered cellular environments are introduced by Siti Hawa Ngalmi et al. Such cross-disciplinary approaches have begun to advance our knowledge of how adhesion signaling is organized and how cells relay information regarding the composition and structure of the external environment into biological activity. In particular, these advances are being driven by novel microscopy technologies and the continuing development of new techniques that allow us to visualize the intricate workings of adhesion-dependent signaling processes. This synopsis gives a glimpse at the current leading edge science published in this special issue of the Journal of Oncology. We hope that these papers inspire interest in multidisciplinary approaches as well as in the identification of novel therapeutics. Claudia D. Andl Ala-Eddin Al Moustafa Therese B. Deramaudt Geraldine M. O’Neill MEDIATORS of INFLAMMATION The Scientific Gastroenterology Journal of World Journal Research and Practice Diabetes Research Disease Markers Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 International Journal of Journal of Immunology Research Endocrinology Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Submit your manuscripts at http://www.hindawi.com BioMed PPAR Research Research International Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Journal of Obesity Evidence-Based Journal of Journal of Stem Cells Complementary and Ophthalmology International Alternative Medicine Oncology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Parkinson’s Disease Computational and Behavioural Mathematical Methods AIDS Oxidative Medicine and in Medicine Research and Treatment Cellular Longevity Neurology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014

Journal

Journal of OncologyHindawi Publishing Corporation

Published: Jan 11, 2011

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