A microscopic cellular assassin, capable of making cancerous kidney cells eat themselves to death, could eventually become a cancer-curing drug, thanks to Auckland University research.
The small molecule, dubbed STF-62247, was discovered by Stanford University researchers, with their findings published in Cancer Cell this month.
But the Auckland research, in collaboration with Stanford University and funded by the United States' National Cancer Institute, is taking the molecule and replicating it into related molecules suited for human drug development.
These new molecules will have increased strike-power, increased water solubility and cause less damage to healthy cells.
The molecule selectively destroys kidney cells by inducing them to "recycle", Auckland University senior research fellow Dr Michael Hay said yesterday.
When cells are depleted of resources or under stress, they naturally recycle bits of nutrients from inside the cell - a process called autophagy. It is normally a survival mechanism for the cells, allowing them to scramble to survive on limited nutrients when times get tough.
Healthy cells can control the autophagy process, by switching it off when it is no longer needed. But about 75 per cent of kidney cancer cells can't. That is because they are either bereft of, or have faulty versions of, a tumour suppressor gene known as the von Hippel-Lindau gene.
The VHL gene is important to the research for two reasons, Dr Hay said.
Firstly, when present in a kidney cell it acts as a brake on cell division, effectively preventing cancer. Secondly, it inhibits a cell's ability to control autophagy.
Therefore, when the STF-62247 molecule induces cells already rich in nutrients to recycle, cells which do not have the ability to turn the process off, autophagy becomes fatal, Dr Hay said.
They continue to recycle until they effectively eat themselves to death, he said.
The resultant drug which the researchers are striving to produce would therefore kill the cancer cells while sparing healthy cells, Dr Hay said. Human trials of the treatment could begin as early as three or four years' time, he said, although much could change before then.