Errors in Mitochondrial DNA the source of cancer spreading

The way in which a cancer spreads is through the process of metastasis, wherein primary cancer cells breaks away from the main tumour, travels through the lymph system or in the bloodstream, settles in a new area and begins to form a new tumour. It is this process which differentiates the less dangerous benign tumours from the deadly malignant kind and preventing it would result in a tumour being easily excisable once identified. A recent study has shown that mutations in Mitochondrial DNA may be responsible for metastasis, and that curing cancer may be as easy as treating a patient with antioxidants.

Mitochondria are organelles within eukaryotic cells that produce energy molecules to fuel cellular processes. They also have their own DNA, referred to as mtDNA, found within the mitochondria itself, rather than the nucleus where most of the cell’s genetic material is stored. This allows the mitochondrion to replicate themselves (with some assistance from the nucleus) depending on the energy needs of the cell, though replication is still controlled by genes within the nucleus. Unfortunately, the protein packaging and self-repair abilities of mtDNA are not as effective as that of nuclear genetic material and so are more susceptible to mutations. It is these mutations that have been suspected of being closely related to metastasis in cancer cells. An earlier study on cancer cells showed that the mitochondria of these cells possessed many more mutations than that of healthy cells, though whether this was a result of the cancer or the cancer was a result of the mutations was unknown.

Researchers at the University of Tsukuba in Japan have recently performed a study on whether mtDNA mutations were responsible for metastasis. The experiment involved swapping the mtDNA of a tumour cell that tends to metastasize with one that does not and injecting the cells into mice. What their results showed was that when these cells were injected into mice the rarely metastasising tumour cells, now containing mtDNA from metastasising tumours, did in fact metastasise, while the originally metastasising tumour cells containing mtDNA from non-metastasising cells did little. This would imply that the basis for tumours metastasising is mtDNA.

Further study showed that the mutations in the mtDNA caused the Mitochondria to produce an excess of reactive oxygen species molecules, which are damaging to DNA. Since mtDNA appears to be the root of metastasis in tumour cells it can be inferred that it is these oxygen species molecules that damage the nuclear genetic material of healthy cells, creating cancer cells. Perhaps most interesting is that these oxygen species molecules can be neutralised with antioxidants and that when mice that had been injected with metastatic tumour cells were treated with these antioxidants, they showed little to no new tumour growth. As a result, antioxidant treatment of malignant cancer has warranted further study.

Original article:

http://sciencenow.sciencemag.org/cgi/content/full/2008/403/1

Image source:

http://www.a3243g.com/image_mitochondria.asp

Kiel Headrick, 4176059