Many studies have pointed out that imbalance of ions may result in irreversible cell damage and cell death through alterations in different intracellular signaling cascades.
Several forms of cell death induced by unbalanced ion homeostasis have been discovered, including ferroptosis and cuproptosis. A better understanding of the molecular determinants of these different modes of cell death may contribute to develop innovative anticancer therapies. For example, ferroptosis, a type of programmed cell death highly dependent on cellular iron concentration, has recently gained remarkable attention with the development of ferroptosis inducers endowed with the capacity to kill cancer cells both in vitro and in vivo. Similarly, elesclomol and disulfiram, two common copper ionophores, were documented to exert cytotoxic effects on cancer cells, confirming the interest for cuproptosis (a copper-triggered modality of mitochondrial cell death) in cancer therapeutics.
Although the above finding are encouraging, there is an urgent need to clarify the underlying molecular mechanisms driving ion-induced cell death and cancer therapy.
Potential topics include but are not limited to the following:
• Ion signaling in cancer cells
• Ion-dependent types of cell death and anticancer treatment
• Unbalanced ion homeostasis as predictive or response biomarkers
• New drugs targeting ion signaling in cancer cell
Many studies have pointed out that imbalance of ions may result in irreversible cell damage and cell death through alterations in different intracellular signaling cascades.
Several forms of cell death induced by unbalanced ion homeostasis have been discovered, including ferroptosis and cuproptosis. A better understanding of the molecular determinants of these different modes of cell death may contribute to develop innovative anticancer therapies. For example, ferroptosis, a type of programmed cell death highly dependent on cellular iron concentration, has recently gained remarkable attention with the development of ferroptosis inducers endowed with the capacity to kill cancer cells both in vitro and in vivo. Similarly, elesclomol and disulfiram, two common copper ionophores, were documented to exert cytotoxic effects on cancer cells, confirming the interest for cuproptosis (a copper-triggered modality of mitochondrial cell death) in cancer therapeutics.
Although the above finding are encouraging, there is an urgent need to clarify the underlying molecular mechanisms driving ion-induced cell death and cancer therapy.
Potential topics include but are not limited to the following:
• Ion signaling in cancer cells
• Ion-dependent types of cell death and anticancer treatment
• Unbalanced ion homeostasis as predictive or response biomarkers
• New drugs targeting ion signaling in cancer cell