Chemotherapy often stops working because it doesn’t kill cancer stem cells that fuel spread of tumours. Scientists have discovered a gene that encourages the spread of breast cancer. They believe the discovery of the gene, RhoC, could lead to new ways to target the behaviour of these deadly cancer cells […]
Chemotherapy often stops working because it doesn’t kill cancer stem cells that fuel spread of tumours.
Scientists have discovered a gene that encourages the spread of breast cancer.
They believe the discovery of the gene, RhoC, could lead to new ways to target the behaviour of these deadly cancer cells and help treat them.
RhoC has previously been shown to promote metastasis – the spread of cancer cells to distant organs, including bone – which is more likely to kill them than a primary breast tumour.
Scientists believe traditional chemotherapy and radiation treatments often become ineffective because they do not kill cancer stem cells that fuel the tumours growth and spread.
However, the researchers say their discovery suggests a new way to target and kill the cancer stem cells.
They looked at breast cancer cell lines that were highly metastic and cell lines from normal breast tissue, finding by inhibiting or over-expressing RhoC, the gene’s expression is necessary to cause metastasis in both cell lines.
The University of Michigan researchers also found RhoC over-expression alone can cause cells to spread, with tests in mice displaying similar results.
They are now studying a small molecule drug to inhibit RhoC, which has shown promising initial results in the lab, but say it will need several years of testing before advancing to clinical trials.
Writing for PLoS ONE, Dr Sofia Merajver said: ‘Targeting the specific molecular cogs driving the cancer stem cell machinery responsible for the cancer spreading has potential for future treatments.
‘Eliminating cancer stem cells may ultimately be necessary to cure certain cancers, but in the meantime, we may be able to manage the cancer stem cell population and the invasive behaviours of these cells by disrupting the molecular machinery, using RhoC as a target.’
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