Gene that spreads breast cancer discovered?
The University of Michigan researchers Scientists claim to have discovered the gene that encourages the spread of breast cancer, paving way for new treatments for the deadly disease.
Scientists have claimed that the discovery of the gene, RhoC, could lead to new ways to target the behaviour of these cancer cells and help treat them.
chemotherapy often stops working because it doesn’t kill cancer stem cells that fuel spread of tumours .
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.
The gene levels increase as breast cancer progresses and higher levels are associated with least survival of the patient. 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.
The researchers, however, say their discovery suggests a new way to target and kill the cancer stem cells.Researchers looked at breast cancer cell lines that were highly metastic comparing them with those from normal breast tissue.
They found that by inhibiting or over-expressing RhoC, the gene’s expression is necessary to cause metastasis in both cell lines. The 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.
Dr Sofia Merajver wrote in PLoS ONE that targeting the specific molecular cogs driving the cancer stem cell machinery responsible for the cancer spreading has potential for future treatments.
The researchers said, eliminating cancer stem cells may ultimately be necessary to cure certain cancers, but in the meantime, they 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.