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Research by the Royal Veterinary College identifies how certain cancer cells resist chemotherapy

Chemotherapy is a drug treatment that uses powerful chemicals to kill fast-growing cells in your body. New research has identified how certain cancer cells resist chemotherapy by creating a protection mechanism. This discovery will now allow scientists to work on how to target these cancer cells for more effective and tailored treatment for patients.

The study, which has been published in the prestigious scientific journal Cell Reports, focussed on ATPase inhibitory factor 1 (IF1), a mitochondrial protein which is expressed in various types of human cancers, and which suppresses programmed cell death (apoptosis), enhancing tumour invasion and chemoresistance. The research group responsible for the discovery was coordinated by Dr Michelangelo Campanella of the Royal Veterinary College (RVC) and included researchers from Kyoto Sangyo University in Japan and the University of Rome TorVergata in Italy. Historically, the scientific literature focussing on IF1 stated that this molecule prevents the consumption of ATP from mitochondria, which are the major cellular source of energy. The study found that IF1, by sparring the consumption ATP, fuels a mechanism of resistance to chemotherapy exploited by cancer cells to evade a chemically induced demise. The hope is that with these research findings, scientists can in future develop IF1 targeting drugs as potential anti-cancer to attack the tumour and increase cancer patients’ survival rates. The experiments were done on human derived cancer cells, meaning the findings can be applied to both the treatment and stratification of animal and human patients pursuing the College’s mission of leadership in comparative physiology and medicine. Commenting on the study, Dr Michelangelo Campanella said: “This study has successfully established the hierarchy between mitochondrial bio-energetics and structure in cancer cells highlighting ATP as an intracellular oncometabolite. We are confident to have, in this way, unveiled a mechanism of mitochondrial structure preservation through the exploitation of retained energy that tangibly increments our understanding of mitochondria orchestrated strategies of resistance to therapy.”