Table 1 Overview of the different chemotherapeutic agents that act through mechanisms related to the MAMs and/or targets localized at the MAMs
Chemotherapy | Target protein | Mechanism of action at MAMs | Functional effect | Cancer type | Reference |
|---|---|---|---|---|---|
Arsenic trioxide | PML | Elevating PML levels, which results in an increased IP3R-mediated ER–mitochondrial Ca2+ transfer | Repression of autophagy | Acute promyelocytic leukemia | |
Cisplatin | Unknown | Increasing ER–mitochondria contact sites and subsequent mitochondrial Ca2+ overload | Apoptosis | Ovarian cancer, non-small cell lung cancer & bladder cancer | |
ABT-737 | Bcl-2 & Bcl-Xl | Alleviating the decrease in IP3R-mediated Ca2+ release by Bcl-2 | (Re)sensitization to cisplatin therapy | Ovarian cancer & cholangiocarcinoma | |
Antagonizing the inhibitory action of Bcl-2 on MAM formation induced by cisplatin | |||||
Resveratrol | ATP synthase | Augmenting mitochondrial Ca2+ due to impaired SERCA activity in the MAMs as a consequence of ATP synthase inhibition | Apoptosis | Broad spectrum | |
Adriamycin | p53 | Increasing SERCA activity and ER Ca2+ loading via p53, which is enriched at ER & MAMs | Apoptosis | Broad spectrum | |
Mitotane | SOAT1 | Provoking the accumulation of toxic cholesterol lipids | Apoptosis | Adrenocortical carcinoma |
