A New Breakthrough in the Fight Against Cancer in Dogs, Cats, and Humans

A study sheds light on interactions within cells and paves the way for potential treatments for neurodegenerative diseases and cancer in both humans and animals.   In an effort to better understand the cellular basis of cancer, researchers at the Royal Veterinary College analyzed interactions within human and animal cells, particularly those involving mitochondria. These organelles, primarily known for their role as the cells’ powerhouses, may play a much more significant role than initially apparent. In fact, mitochondria actively participate in the reprogramming of cells in mammals. In response to disturbances, they can communicate back to the nucleus to regulate gene transcription. This process is known as the mitochondrial retrograde response (MRR). However, this influence on cellular gene expression—while important for cellular adaptation to stress—can be hijacked and exploited, particularly in the pathogenesis of uncontrolled cell proliferation, more commonly known as cancer. By analyzing feline, canine, and human cancer cells—ranging in aggressiveness—researchers were able to demonstrate that the MRR is facilitated by contact sites between mitochondria and the nucleus that enable communication. And depending on the cells’ sensitivity to chemotherapy—and thus the ability to control the disease—a varying number of contact sites are found between the mitochondria and the nucleus. This discovery represents a giant leap forward in understanding mitochondria-nucleus communication and, more broadly, intracellular signaling. The authors suggest that this interaction could be targeted and controlled, which would pave the way for new therapeutic strategies in the fight against many diseases, including cancer. This is the first study of its kind to reveal the interaction between mitochondria and the nucleus as a regulated process that can be pharmacologically controlled. The impact of this discovery likely extends beyond an advanced understanding of the physiology and pathology of mammalian cells, the authors state. “This is truly revolutionary, as it would allow us to develop ways to correct mitochondrial signaling in pathological conditions such as cancer and neurodegeneration.”