Mitochondria discovery prompts bone marrow investigation
06 August 2015, Cancer
The world-first discovery earlier this year of mitochondrial transfer to tumour cells has created a wave of local and international follow-up. The phrase research begets research has never been more apt as a team at the Malaghan Institute begin investigations into mitochondrial movement between cells following bone marrow transplantation.
Professor Mike Berridge is naturally excited, Our earlier work demonstrated transfer of genes from healthy cells to cancer cells without mitochondrial DNA. Cancer cells with damaged mitochondria acquire replacements from surrounding healthy cells, restoring respiration and tumour forming ability. In lay persons terms the tumour cells got back their energy generators. Using fluorescent probes and mitochondrial DNA sequencing we saw replacement mitochondria essential for respiration tracking between cells through membrane nanotubes. (See the top image on the right.)
The possibilities for research are enormous. We are now trying to understand how to stop transfer of these energy-producing engines to cancer cells with mitochondrial DNA damage caused by radiation or drug treatment. We are also interested in promoting mitochondrial movement to cells that are fatigued, damaged or dying. What Rob (Dr Robert Weinkove, part-time Malaghan researcher and haematologist at Wellington Hospital) and I will look at is the triggers that drive this process. We need to understand the basics as a foundation for future work. Mike explains further, There is existing evidence of cytoplasmic bridges (See bottom image on right), resembling membrane nanotubes, joining cells that form red blood cells. These bridges look remarkably like the nanotubes we see with tumour cells. They may be involved in optimising haemoglobin production in red cells which carry oxygen for respiration. But there is so much to be learned. For example, we dont yet know whether damage resulting from radiation or chemotherapy in patients with leukaemia is a trigger for mitochondria movement, or if it occurs naturally.