Hanne Verswyvel

Chapter 5 │ Page 162 also been explored to kill cancerous cells by stimulating their anti-tumorigenic property. Strategies that leverage GJs ability to facilitate the transport of reactive oxygen and nitrogen species (RONS) between adjacent cells can cause cellular stress and death via oxidative damage to proteins and membrane lipids [29-31]. An increasing body of experimental evidence demonstrates that oxidative stress modulates channel gating (pore opening/closing) of GJs, and that in turn facilitates the tra ic of RONS to the cell interior [32,33]. Therefore, oxidative stress-inducing therapies as novel anti-cancer modality for modulating GJs, are gaining attention, which include photodynamic therapy (PDT) [34,35] and non-thermal plasma (NTP) [36,37]. Figure 1: Schematic representation of GJs and e ector functions between di erent cell types. GJs are key mediators of intercellular communication. Moreover, a previously underestimated role of GJs in alternative pathways for immune regulation and activation has been recently described (see section 6 for explanation). (A) Tumor cell transfers tumor promoting signals to another tumor cell via homologous GJs, increasing tumoral e ects. Besides, homologous GJs also transfer death signals (Ca2+) between tumor cells, inducing tumor cell death. (B) Tumor cell transfers Ag peptides to DC via GJs, leading to antigen cross-presentation by DC. Further, DC presents Ag peptides and transfers secondary

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