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Fig. 6. Hypothetical mechanisms of tissue polarity as a non-cell-autonomous tumor suppressor. (A) In normal tissues, cells use their AJCs to link internal cell-polarity mechanisms (asymmetrically localized cell-polarity proteins) with polarized 3D tissue organization. (B) Pro-tumorigenic changes in the mutant cells might disrupt internal cell-polarity mechanisms (see Fig. 3). If mutant cells express AJC proteins, the normal cell neighbors could use AJCs to maintain polarity and attenuate the malignant phenotype of the mutant cells. In this context, both 3D tissue polarity and AJC proteins have an important tumor-suppression function. (C) When the mutant cell is unable to form AJCs with its neighbors, an alternative 3D-mediated tumor-suppression mechanism may be engaged. Epithelial cells use AJCs as a biosensor of the external cellular microenvironment (Lien et al., 2006). Normal cells will treat the AJC-negative mutant as an empty space and may exfoliate it by an actin-myosin-mediated `purse-string' wound-healing mechanism (Brock et al., 1996; Danjo and Gipson, 1998). Only when the mechanisms describend in B and C both fail will the mutant cells progress and form the tumor.

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