Hanne Verswyvel

Chapter 5 │ Page 174 [115]. Another explanation for the depletion of Cxs in cancer cells is based on transcriptional and post-translational modifications, such as phosphorylation, acetylation and palmitoylation [116], and methylation [117]. It was demonstrated that many growth factors, oncogenes, and tumor-promoting chemicals were potent inducers of Cx phosphorylation, which is often associated with the GJ inhibition [84]. The mechanism underlying the tumor-suppressive functions of Cxs and GJs are highly complex, involving several properties intrinsic to Cxs proteins and other proteins surrounding it. Di erent electrical potential of GJIC, pore diameters in the connexons, and post-translational modifications of the Cxs conformations may also be responsible for changes in anti-tumorigenic properties of GJs. Such changes must be considered at both cellular and molecular levels for novel therapy development. To summarize, Cxs and GJs can act as pro- and anti-tumorigenic agents, depending on many factors such as GJs, cancer and tumor (Figure 4). Figure 4: Factors influencing the tumor-promoting and tumor-suppressing properties of Cxs and GJs.

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