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First-in-Class Anti-Cancer Nanoparticle Copper(Ii) Phosphorus Dendrimers as Pro-Apoptotic Bax Activators
Published in Anne-Marie Caminade, Cédric-Olivier Turrin, Jean-Pierre Majoral, Phosphorus Dendrimers in Biology and Nanomedicine, 2018
Serge Mignani, Nabil El Brahmi, Thierry Cresteil, Jean-Pierre Majoral
An alternative caspase-independent apoptosis pathway involves the release of apoptosis inducing factor (AIF) from the mitochondria and its translocation to the nucleus. To assess this possible mechanism, cells were treated with 1G3 and 1G3-Cu, and mitochondrial, nuclear, and cytosolic subfractions were prepared and used for immunochemical determinations. In cells treated with the vehicle, AIF was mostly detected in the mitochondrial compartment. Following exposure to doxorubicin and cisplatin, the AIF content was strikingly reduced in the mitochondria and concomitantly increased in the cytosol (not shown) and nuclei ( .7B). With 1G3, the AIF mitochondrial content was moderately reduced while increased in nuclei on a dose-dependent basis. A similar dose-dependent translocation was noticed with 1G3-Cu but with a higher efficiency resulting in an almost complete transfer of AIF from mitochondria to nuclei.
The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
There also exists a caspase-independent apoptotic pathway that is mediated by AIF (Apoptosis-Inducing Factor) [24]. AIF is phylogenetically an old flavoprotein observed in the mitochondrial intermembrane. Upon lethal stimuli, AIF translocates from mitochondria to the nucleus. It binds to DNA and mediates caspase-independent chromatin condensation and large scale DNA fragmentation [25, 26].
Combined treatment with auranofin and trametinib induces synergistic apoptosis in breast cancer cells
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Min-Kyung Joo, Sangyun Shin, Dong-Jin Ye, Hong-Gyu An, Tae-Uk Kwon, Hyoung-Seok Baek, Yeo-Jung Kwon, Young-Jin Chun
To identify the molecular mechanism underlying the impact of combining auranofin and trametinib, nuclear translocation of AIF from mitochondria was examined. AIF is a direct inducer of apoptosis associated with PARP cleavage and mitochondrial apoptosis. Confocal microscopy demonstrated that combination treatment promoted translocation of AIF into the nucleus, but auranofin or trametinib alone failed to alter nuclear translocation of AIF (Figure 5). Data suggested that combination exposure with auranofin and trametinib produced synergistic apoptosis by enhancing translocation of AIF from mitochondria, by increasing the permeability of the mitochondrial outer membrane.