RVC-led study analyses cancer cells in humans and animals
A recent study that found a new interaction within cells has opened the door for new potential treatments of neurological conditions in humans and animals such as cancer and neurodegeneration.
The study was led by Professor Michelangelo Campanella, chair in Pharmacology and head of the Mitochondrial Cell Biology and Pharmacology Research Unit at the Royal Veterinary College (RVC).
Researchers analysed breast cancer cells of varying levels of aggressiveness from humans, dogs and cats. According to the study, the evolution of the breast cancer in these three species meant that their susceptibility to chemotherapy was found to be associated with the amount of contact sites between mitochondria and nuclei.
The study used multiple molecular pharmacology protocols to control the interaction between mitochondria and nuclei, as well as florescent imaging to map the interaction and transmission electron microscopy to picture the ultrastructure of Nucleus-Associated Mitochondria (NAM).
According to the authors, this discovery advances the understanding of mitochondrion-to-nucleus communication and intracellular signalling. Suggesting that this interaction inside cells can be targeted and controlled, allowing for new enhanced strategies for fighting diseases.
Professor Campanella said: “This study is the first of its kind to unveil the association between the mitochondrion and nucleus to be a regulated process and can be used to identify how this interplay can be pharmacologically controlled.
“The impact of this discovery is likely bigger than the advanced comprehension of mammalian cells physiology and pathology, embracing aspects of evolution. The co-existence of distinct DNAs is just partially understood and how genes from the mitochondria are transferred to genomic DNA is completely unknown.
“Our research group has now started investigating the molecular determinants of membrane tethering at NAM and the involvement of these inter-organellar communication in several disease models.
"This is truly ground-breaking as it will allow us to develop ways of correcting mitochondrial signalling in pathological conditions including cancer and neurodegeneration.”
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