In the extracellular environment, TG2 can modify the extracellular matrix proteins and alter cell-cell (homotypic) and cell-matrix (heterotypic) interactions [14].
The decrease in E-cadherin expression after RhoB depletion would be predicted to alter cell-cell junction organization.
These studies also showed that KAI1 transfectants exhibited enhanced calcium-independent aggregation, suggesting that KAI1 might alter cell-cell interactions.
This suggests the lipoprotein environment of circulating and sub-endothelial monocytes in Type 2 diabetes could promote altered shedding of membrane-bound cytokines, receptors and adhesion molecules and alter cell-cell interactions.
Proteins encoded by MMP and MT-MMP genes can alter cell-cell and cell-ECM junctions; both mediate the release and activation of autocrine or paracrine signaling molecules such as angiogenic activators as well as activate or deactivate cell surface receptors, promoting invasiveness and metastasis [ 34].
Radiation can also induce non-targeted effects - altered cytokines and signaling that affect the cellular composition and microenvironment of irradiated tissues [ 1], and non-mutational, but heritable changes that alter cell-cell interactions and induce persistent phenotypes associated with malignant progression [ 2- 4].
EMT in cultured islet beta cells is likely a consequence of cell dissociation from the normal epithelial structure, resulting in altered cell-cell and cell-matrix contacts.
Cell characteristics in cancer affected during Epithelial-mesenchymal transition resulting in altered cell-cell and cell-matrix interactions, cell motility and invasiveness [ 33].
The cell characteristics are highly affected during the EMT, resulting in altered cell-cell and cell-matrix interactions, and increased cell motility and invasiveness.
For example, altered cell-cell (homotypic) and cell-ECM (heterotypic) interactions that are considered critical in the development and progression of cancer can be modulated by TG2.
Spatially, ST3 mRNA and protein are expressed in the fibroblasts within the connective tissue [ 114, 119], suggesting that ST3 is one of the connective tissue genes that affect epithelial transformation by altering cell-cell and cell-ECM interactions.
