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      Cancer metastases: challenges and opportunities

      review-article
      Author(s): *
      Publication date (Electronic):
      Journal: Acta Pharmaceutica Sinica. B
      Publisher: Elsevier
      Keywords: BM, basement membrane, CAFs, cancer-associated fibroblasts, CAMs, cell adhesion molecules, CAT, collective amoeboid transition, CCL2, chemokine (C–C motif) ligand 2, CCR3, chemokine receptor 3, Col, collagen, COX2, cyclooxygenase 2, CSF-1, chemokine colonystimulating factor–1, CTGF, connective tissue growth factor, CXCR2, chemokine receptor type 2, DISC, death-inducing signaling complex, ECM, extracellular matrix, EGF, epidermal growth factor, EGFR, EGF receptor, EMT, epithelial–mesenchymal transition, FAK, focal adhesion kinase, FAs, focal adhesions, FGF, fibroblast growth factor, FN, fibronectin, HA, hyaluronan, HGF, hepatocyte growth factor, HIFs, hypoxia-inducible factors, IKK, IκB kinase, JAK, the Janus kinases, LN, laminin, MAPK, mitogen-activated protein kinase, MAT, mesenchymal to amoeboid transition, MET, mesenchymal–epithelial transition, MMPs, matrix metalloproteinases, PDGF, platelet-derived growth factor, PI3K, phosphatidylinositol 3-kinase, STATs, signal transducers and activators of transcription, TAMs, tumor-associated macrophages, TGF-β, transforming growth factor β, TME, tumor microenvironment, VCAMs, vascular cell adhesion molecules, VEGF, vascular endothelial growth factor, VN, vitronectin, Metastasis, Detachment, Migration, Invasion, Adhesion, Cancer

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          Abstract

          Cancer metastasis is the major cause of cancer morbidity and mortality, and accounts for about 90% of cancer deaths. Although cancer survival rate has been significantly improved over the years, the improvement is primarily due to early diagnosis and cancer growth inhibition. Limited progress has been made in the treatment of cancer metastasis due to various factors. Current treatments for cancer metastasis are mainly chemotherapy and radiotherapy, though the new generation anti-cancer drugs (predominantly neutralizing antibodies for growth factors and small molecule kinase inhibitors) do have the effects on cancer metastasis in addition to their effects on cancer growth. Cancer metastasis begins with detachment of metastatic cells from the primary tumor, travel of the cells to different sites through blood/lymphatic vessels, settlement and growth of the cells at a distal site. During the process, metastatic cells go through detachment, migration, invasion and adhesion. These four essential, metastatic steps are inter-related and affected by multi-biochemical events and parameters. Additionally, it is known that tumor microenvironment (such as extracellular matrix structure, growth factors, chemokines, matrix metalloproteinases) plays a significant role in cancer metastasis. The biochemical events and parameters involved in the metastatic process and tumor microenvironment have been targeted or can be potential targets for metastasis prevention and inhibition. This review provides an overview of these metastasis essential steps, related biochemical factors, and targets for intervention.

          Graphical abstract

          Cancer metastasis is the major cause of cancer morbidity and mortality, and accounts for about 90% of cancer deaths. Limited progress has been made in the treatment of cancer metastasis due to various factors. This review is aimed to provide an overview of the metastasis process and targets for intervention with a focus on cancer cell detachment, migration, invasion and adhesion. It is hoped that this review can serve as a lead for readers who are interested in cancer metastasis and intervention.

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          CD44: from adhesion molecules to signalling regulators.

          Helmut Ponta, Larry Sherman, Peter A Herrlich (2003)
          Cell-adhesion molecules, once believed to function primarily in tethering cells to extracellular ligands, are now recognized as having broader functions in cellular signalling cascades. The CD44 transmembrane glycoprotein family adds new aspects to these roles by participating in signal-transduction processes--not only by establishing specific transmembrane complexes, but also by organizing signalling cascades through association with the actin cytoskeleton. CD44 and its associated partner proteins monitor changes in the extracellular matrix that influence cell growth, survival and differentiation.
          Article 0 comments Cited 611 times – based on 0 reviews     Review now
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            The tumour-induced systemic environment as a critical regulator of cancer progression and metastasis.

            Sandra S McAllister, Robert Weinberg (2014)
            Recent pre-clinical and clinical research has provided evidence that cancer progression is driven not only by a tumour's underlying genetic alterations and paracrine interactions within the tumour microenvironment, but also by complex systemic processes. We review these emerging paradigms of cancer pathophysiology and discuss how a clearer understanding of systemic regulation of cancer progression could guide development of new therapeutic modalities and efforts to prevent disease relapse following initial diagnosis and treatment.
            Article 0 comments Cited 407 times – based on 0 reviews     Review now
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              CXCR4: a key receptor in the crosstalk between tumor cells and their microenvironment.

              Jan A Burger, Thomas J Kipps (2006)
              Signals from the microenvironment have a profound influence on the maintenance and/or progression of hematopoietic and epithelial cancers. Mesenchymal or marrow-derived stromal cells, which constitute a large proportion of the non-neoplastic cells within the tumor microenvironment, constitutively secrete the chemokine stromal cell-derived factor-1 (SDF-1/CXCL12). CXCL12 secretion by stromal cells attracts cancer cells, acting through its cognate receptor, CXCR4, which is expressed by both hematopoietic and nonhematopoietic tumor cells. CXCR4 promotes tumor progression by direct and indirect mechanisms. First, CXCR4 is essential for metastatic spread to organs where CXCL12 is expressed, and thereby allows tumor cells to access cellular niches, such as the marrow, that favor tumor-cell survival and growth. Second, stromal-derived CXCL12 itself can stimulate survival and growth of neoplastic cells in a paracrine fashion. Third, CXCL12 can promote tumor angiogenesis by attracting endothelial cells to the tumor microenvironment. CXCR4 expression is a prognostic marker in various types of cancer, such as acute myelogenous leukemia or breast carcinoma. Promising results in preclinical tumor models indicate that CXCR4 antagonists may have antitumor activity in patients with various malignancies. Collectively, these observations reveal that CXCR4 is an important molecule involved in the spread and progression of a variety of different tumors. As such, CXCR4 antagonists, although initially developed for treatment of AIDS, actually may become effective agents for the treatment of neoplastic disease.
              Article 0 comments Cited 296 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Xiangming Guan
                Journal
                Journal ID (nlm-ta): Acta Pharm Sin B
                Journal ID (iso-abbrev): Acta Pharm Sin B
                Title: Acta Pharmaceutica Sinica. B
                Publisher: Elsevier
                ISSN (Print): 2211-3835
                ISSN (Electronic): 2211-3843
                Publication date PMC-release: 08 September 2015
                Publication date (Print): September 2015
                Publication date (Electronic): 08 September 2015
                Volume: 5
                Issue: 5
                Pages: 402-418
                Affiliations
                [0005]Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007, USA
                Author notes
                [* ]Tel.: +1 605 6885314; fax: +1 605 6885993. Xiangming.guan@ 123456sdstate.edu
                Article
                Publisher ID: S2211-3835(15)00109-4
                DOI: 10.1016/j.apsb.2015.07.005
                PMC ID: 4629446
                PubMed ID: 26579471
                SO-VID: 04afc964-3f5b-4d73-8754-9d00be2cedb3
                Copyright © © 2015 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
                License:

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

                History
                Date received : 8 May 2015
                Date accepted : 2 June 2015
                Categories
                Subject: Review

                Keywords: bm, basement membrane,cafs, cancer-associated fibroblasts,cams, cell adhesion molecules,cat, collective amoeboid transition,ccl2, chemokine (c–c motif) ligand 2,ccr3, chemokine receptor 3,col, collagen,cox2, cyclooxygenase 2,csf-1, chemokine colonystimulating factor–1,ctgf, connective tissue growth factor,cxcr2, chemokine receptor type 2,disc, death-inducing signaling complex,ecm, extracellular matrix,egf, epidermal growth factor,egfr, egf receptor,emt, epithelial–mesenchymal transition,fak, focal adhesion kinase,fas, focal adhesions,fgf, fibroblast growth factor,fn, fibronectin,ha, hyaluronan,hgf, hepatocyte growth factor,hifs, hypoxia-inducible factors,ikk, iκb kinase,jak, the janus kinases,ln, laminin,mapk, mitogen-activated protein kinase,mat, mesenchymal to amoeboid transition,met, mesenchymal–epithelial transition,mmps, matrix metalloproteinases,pdgf, platelet-derived growth factor,pi3k, phosphatidylinositol 3-kinase,stats, signal transducers and activators of transcription,tams, tumor-associated macrophages,tgf-β, transforming growth factor β,tme, tumor microenvironment,vcams, vascular cell adhesion molecules,vegf, vascular endothelial growth factor,vn, vitronectin,metastasis,detachment,migration,invasion,adhesion,cancer
                Data availability:
                Keywords: bm, basement membrane, cafs, cancer-associated fibroblasts, cams, cell adhesion molecules, cat, collective amoeboid transition, ccl2, chemokine (c–c motif) ligand 2, ccr3, chemokine receptor 3, col, collagen, cox2, cyclooxygenase 2, csf-1, chemokine colonystimulating factor–1, ctgf, connective tissue growth factor, cxcr2, chemokine receptor type 2, disc, death-inducing signaling complex, ecm, extracellular matrix, egf, epidermal growth factor, egfr, egf receptor, emt, epithelial–mesenchymal transition, fak, focal adhesion kinase, fas, focal adhesions, fgf, fibroblast growth factor, fn, fibronectin, ha, hyaluronan, hgf, hepatocyte growth factor, hifs, hypoxia-inducible factors, ikk, iκb kinase, jak, the janus kinases, ln, laminin, mapk, mitogen-activated protein kinase, mat, mesenchymal to amoeboid transition, met, mesenchymal–epithelial transition, mmps, matrix metalloproteinases, pdgf, platelet-derived growth factor, pi3k, phosphatidylinositol 3-kinase, stats, signal transducers and activators of transcription, tams, tumor-associated macrophages, tgf-β, transforming growth factor β, tme, tumor microenvironment, vcams, vascular cell adhesion molecules, vegf, vascular endothelial growth factor, vn, vitronectin, metastasis, detachment, migration, invasion, adhesion, cancer

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