Cell polarity1/17/2024 ![]() Integrins and cadherins join forces to form adhesive networks. Cell polarity and cancer-cell and tissue polarity as a non-canonical tumor suppressor. Regulation of cell polarity during epithelial morphogenesis. Megaintestine in claudin-15-deficient mice. Sticky business: orchestrating cellular signals at adherens junctions. Regulation of asymmetric cell division in the epidermis. Planar cell polarity signaling: from fly development to human disease. Cell polarity in eggs and epithelia: parallels and diversity. Hallmarks of cancer: the next generation. Evidence for the stem or progenitor cell-of-origin model has been provided for some carcinomas or specific subtypes of carcinomas however, this seems to be unlikely or has not been well defined for several others. Two theories of tumour initiation have been postulated one proposes that some tumours arise from normal adult stem or progenitor cells that have gone awry, and the other postulates that they arise from differentiated cells that acquire self-renewal capabilities. The genes that control epithelial cell polarity also regulate spindle orientation and the symmetry of cell divisions in stem cells.Įpithelial tumours are highly heterogeneous, and the cell-of-origin that can initiate tumorigenesis is an area of extensive study. During differentiation stem cells reorient their mitotic spindles and divide asymmetrically in order to generate the specialized cells that drive epithelial function and homeostasis. The maintenance of most adult epithelial tissues relies on the presence of polarized stem cells, which self-renew through symmetric cell divisions. The LKB1–AMPK–mTOR pathway, which is a molecular link between polarity and the metabolic status of a cell, is essential in the process of tumorigenesis. Recent studies have provided evidence that the cell polarity regulators lethal (2) giant larvae homologue (LGL also known as LLGL), atypical protein kinase C (aPKC) and crumbs homologue (CRB), and the adherens junctions components E-cadherin–α-catenin or E-cadherin–β-catenin regulate the Hippo pathway in mammalian and Drosophila melanogaster epithelial cells. The components of the evolutionarily conserved Hippo pathway function as important tumour suppressors. Accumulating evidence indicates that epithelial cell polarity cues and polarized cell divisions causally contribute to restrict carcinoma formation.Ĭell polarity proteins crosstalk with signalling pathways that regulate cell growth and proliferation, including the WNT and Hippo pathways, and liver kinase B1 (LKB1)–mTOR-dependent energy metabolism. Loss of epithelial cell polarity - through deregulation of these proteins - is crucial for cancer cell invasion and advanced tumour progression. The proteins that finely control epithelial cell polarity are known as tumour suppressors or proto-oncoproteins. ![]()
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