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  • Laminin-332-integrin interaction: a target for cancer therapy?
  • Tsuruta D; Kobayashi H; Imanishi H; Sugawara K; Ishii M; Jones JC
  • Curr Med Chem 2008[]; 15 (20): 1968-75
  • For many years, extracellular matrix (ECM) was considered to function as a tissue support and filler. However, we now know that ECM proteins control many cellular events through their interaction with cell-surface receptors and cytoplasmic signaling pathways. For example, they regulate cell proliferation, cell division, cell adhesion, cell migration, and apoptosis. We focus in this review on a laminin isoform, laminin-332 (formerly termed laminin-5), a major component of the basement membrane (BM) of skin and other epithelial tissues. It is composed of 3 subunits (alpha3beta3 and gamma3 and interacts with at least two integrin receptors expressed by epithelial cells (alpha3beta1 and alpha6beta4 integrin. Mutations in either laminin-332 or integrin alpha6beta4 result in junctional epidermolysis bullosa, a blistering skin disease, while targeting of laminin-332 by autoantibodies in cicatricial pemphigoid leads to dysadhesion of epithelial cells from their underlying connective tissue. Abnormal expression of laminin-332 and its integrin receptors is also a hallmark of certain tumor types and is believed to promote invasion of colon, breast and skin cancer cells. Moreover, there is emerging evidence that laminin-332 and its protease degradation products are not only found at the leading front of several tumors but also likely induce and/or promote tumor cell migration. Thus, in this review, we focus specifically on the role of laminin-332 and its integrin receptors in adhesion, proliferation, and migration/invasion of cancer cells. Finally, we discuss strategies for the development of laminin-332-based antagonists for the treatment of malignant tumors.
  • |Animals[MESH]
  • |Cell Adhesion Molecules/chemistry/*metabolism[MESH]
  • |Extracellular Matrix/*metabolism[MESH]
  • |Humans[MESH]
  • |Integrins/*metabolism[MESH]
  • |Metalloproteases/metabolism[MESH]
  • |Neoplasms/blood supply/*drug therapy/*metabolism[MESH]
  • |Neovascularization, Pathologic[MESH]
  • |Protein Kinases/metabolism[MESH]
  • |Signal Transduction[MESH]

  • *{{pmid18691052}}
    *<b>[ Laminin-332-integrin interaction: a target for cancer therapy?]</b> Curr Med Chem 2008; 15(20) ; 1968-75 Tsuruta D; Kobayashi H; Imanishi H; Sugawara K; Ishii M; Jones JC


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    Curr Med Chem

    1968 20.15 2008