For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phag...

/pdf/the-nox-family-of-ros-generating-nadph-oxidases-physiology-zjc88zvh59.pdf

The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology

Reactive oxygen species

Phosphoinositide 3-kinases (PI3Ks) function early in intracellular signal transduction pathways and affect many biological functions. A further level of complexity derives from the existence of eight PI3K isoforms, which are divided into class I, class II and class III PI3Ks. PI3K signalling has been implicated in metabolic control, immunity, angiogenesis and cardiovascular homeostasis, and is one of the most frequently deregulated pathways in cancer. PI3K inhibitors have recently entered clinical trials in oncology. A better understanding of how the different PI3K isoforms are regulated and control signalling could uncover their roles in pathology and reveal in which disease contexts their blockade could be most beneficial.

The emerging mechanisms of isoform-specific PI3K signalling

Mitochondria are the cells' powerhouse, but also their suicidal weapon store. Dozens of lethal signal transduction pathways converge on mitochondria to cause the permeabilization of the mitochondrial outer membrane, leading to the cytosolic release of pro-apoptotic proteins and to the impairment of the bioenergetic functions of mitochondria. The mitochondrial metabolism of cancer cells is deregulated owing to the use of glycolytic intermediates, which are normally destined for oxidative phosphorylation, in anabolic reactions. Activation of the cell death machinery in cancer cells by inhibiting tumour-specific alterations of the mitochondrial metabolism or by stimulating mitochondrial membrane permeabilization could therefore be promising therapeutic approaches.

/pdf/targeting-mitochondria-for-cancer-therapy-2ezqvlkpfu.pdf

Targeting mitochondria for cancer therapy

Complex biological systems and cellular networks may underlie most genotype to phenotype relationships. Here, we review basic concepts in network biology, discussing different types of interactome networks and the insights that can come from analyzing them. We elaborate on why interactome networks are important to consider in biology, how they can be mapped and integrated with each other, what global properties are starting to emerge from interactome network models, and how these properties may relate to human disease.

Interactome networks and human disease

https://febs.onlinelibrary.wiley.com/doi/epdf/10.1016/S0014-5793%2802%2903691-8

Paclitaxel targets mitochondria upstream of caspase activation in intact human neuroblastoma cells.

https://hal-amu.archives-ouvertes.fr/hal-01481645/document

The effects of caffeic, coumaric and ferulic acids on proliferation, superoxide production, adhesion and migration of human tumor cells in vitro.

Synthesis and cytotoxicity evaluation of some benzimidazole-4,7-diones as bioreductive anticancer agents

Nox1-dependent superoxide production controls colon adenocarcinoma cell migration.

https://hal-amu.archives-ouvertes.fr/hal-01474951/document

Hervé Kovacic

Papers

Paclitaxel targets mitochondria upstream of caspase activation in intact human neuroblastoma cells.

The effects of caffeic, coumaric and ferulic acids on proliferation, superoxide production, adhesion and migration of human tumor cells in vitro.

Synthesis and cytotoxicity evaluation of some benzimidazole-4,7-diones as bioreductive anticancer agents

Nox1-dependent superoxide production controls colon adenocarcinoma cell migration.

Rutin inhibits proliferation, attenuates superoxide production and decreases adhesion and migration of human cancerous cells.