Apicobasal polarity and its role in cancer progression

  title={Apicobasal polarity and its role in cancer progression},
  author={Priscilla J.K.P. Lo and Hannah Hawrot and Marios Georgiou},
  booktitle={Biomolecular concepts},
Abstract Appropriate establishment and maintenance of cell polarity is essential for normal development and homeostasis. The vast majority of human cancers originate from epithelial tissues and tumour cell invasion and metastasis are the major cause of mortality in human cancers. Invading cells demonstrate loss of cell polarity, loss of epithelial cell-cell adhesions and tissue disorganisation. We examine the growing evidence linking loss of apicobasal polarity with tumour progression. 
ignalling networks in focus hoGTPase signalling at epithelial tight junctions : Bridging the GAP etween polarity and cancer
The establishment and maintenance of epithelial polarity must be correctly controlled for normal development and homeostasis. Tight junctions (TJ) in vertebrates define apical and basolateralExpand
A Genetic Analysis of Tumor Progression in Drosophila Identifies the Cohesin Complex as a Suppressor of Individual and Collective Cell Invasion
Using the genetic amenability of Drosophila melanogaster, a detailed systematic loss-of-function analysis was carried out to identify conserved genes that enhance or suppress epithelial tumor progression and the discovery of functional cooperative regulators of invasion and the establishment of a network of conserved invasion suppressors. Expand
The multifarious regulation of the apical junctional complex
This review will focus on the tight and adherens junctions, constituents of the apical junctional complex, and aims to provide a comprehensive overview of the complex signalling that underlies junction assembly, integrity and plasticity. Expand
RhoGTPase signalling at epithelial tight junctions: Bridging the GAP between polarity and cancer
  • C. Zihni, S. Terry
  • Biology, Medicine
  • The international journal of biochemistry & cell biology
  • 2015
It is determined that the expression, localization or stability of a variety of these adaptor proteins is altered in various cancers, potentially representing an important mechanistic link between loss of polarity and cancer. Expand
The interdependence of the Rho GTPases and apicobasal cell polarity
The relationships between the Rho family GTPases and epithelial AB polarization events are reviewed, focusing on the 3 best-characterized members: Rho, Rac and Cdc42. Expand
An apicobasal gradient of Rac activity determines protrusion form and position
A mechanism by which polarity proteins can spatially regulate Rac activity and the actin cytoskeleton to ensure correct epithelial cell shape and prevent epithelial-to-mesenchymal transitions is demonstrated. Expand


Role of the polarity determinant crumbs in suppressing mammalian epithelial tumor progression.
A role for mammalian polarity determinants in suppressing tumorigenesis that may be analogous to the well-studied polarity tumor suppressor mechanisms in Drosophila is suggested. Expand
Epithelial polarity and proliferation control: links from the Drosophila neoplastic tumor suppressors.
  • D. Bilder
  • Biology, Medicine
  • Genes & development
  • 2004
Mammalian epithelial tumors lose polarity as they progress toward malignancy, but whether polarity loss might causally contribute to cancer has remained unclear. In Drosophila, mutations in theExpand
Aberrant overexpression of the cell polarity module scribble in human cancer.
It is shown that Scrib is nearly universally overexpressed in cultured tumor cell lines and genetically disparate cancer patient series compared with matched normal tissues in vivo, revealing a previously unrecognized exploitation of Scrib for aberrant tumor cell motility and invasion. Expand
Cell Polarity in Eggs and Epithelia: Parallels and Diversity
The similarities and differences between the polarity mechanisms in eggs and epithelia are highlighted and the prospects for future studies on how cortical polarity interfaces with other cellular processes, such as morphogenesis, exocytosis, and lipid signaling, are highlighted. Expand
Epithelial-Mesenchymal Transitions in Development and Disease
The mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis. Expand
scribble mutants promote aPKC and JNK-dependent epithelial neoplasia independently of Crumbs
Different aPKC and JNK-dependent pathways through which loss of Scrib promotes tumourigenesis in Drosophila are demonstrated, likely to have a direct relevance to the way in which human Scrib can similarly restrain an oncogene-mediated transformation and, more generally, on how the outcome of oncogenic signalling can be profoundly perturbed by defects in apico-basal epithelial cell polarity. Expand
Deregulation of Scribble Promotes Mammary Tumorigenesis and Reveals a Role for Cell Polarity in Carcinoma
It is demonstrated that scribble inhibits breast cancer formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disrupting morphogenesis and inhibiting cell death. Expand
Loss of Cell Polarity Drives Tumor Growth and Invasion through JNK Activation in Drosophila
The finding that context-dependent alterations promote both tumor growth and metastatic behavior suggests that metastasis- Promoting mutations may be selected for based primarily on their growth-promoting capabilities. Expand
Epithelial polarity: The ins and outs of the fly epidermis
Light is shed on how apical-basal polarity is generated during cellularization in Drosophila, when around 6000 epithelial cells are created synchronously from a syncytium. Expand
Involvement of E‐cadherin, β‐catenin, Cdc42 and CXCR4 in the progression and prognosis of cutaneous melanoma
The development of melanoma may be viewed as a consequence of the disruption of homeostatic mechanisms in the skin of the original site as well as the migration of tumour cells from their original location to a secondary site. Expand