Two of the most enticing ideas in cells biology have recently converged to create a paradigm shift of epic proportions. The first is that not only is it possible for mitochondria to emigrate from their host cell, they are in fact exchanged among cells much more regularly than has ever been imagined. The second is that while happenstance mutations are clearly associated with different aspects of a litany of cancers, the canonical force consistently driving tumor initiation, progression, and metastasis is now broadly understood to be the metabolic fickleness of their mitochondria. Mike Berridge is one of a handful of researchers firmly planted at the intersection of these two now ineluctable conclusions. As an author on a recent review in Cancer Research on the horizontal transfer of mitochondrial DNA (mtDNA), he adds much needed flesh to the first order simplification that cancer is merely a mitochondrial respiratory insufficiency. Most poignantly, in noting that the hidden force driving tumor-formation forward can more generally be understood to be the reacquisition of once lost mitochondrial function, new therapeutic opportunities immediately present themselves.
Of particular note Berridge found that the apparent need and ability of mitochondria-free primary tumor lines to re-assemble functional respirasomes, the supercomplexes responsible for respiration, differed according to cancer type. For example, breast cancer cells were found to have a unique 'threshold' level of respiration that was different from melanoma cells. Nover anticancer agents could in theory be designed to target specific components in more respiration-dependant cancer cells while leaving other cell types unscathed.