A team of researchers at Dana-Farber Cancer Institute has uncovered a protein in cancer cells, which could sensitise cancerous tumours to radiation.
In an attempt to make radiation therapy more effective and cancer cells more sensitive to several cancer drugs, the researchers used a molecular tool to lower the cells' cyclin D1 levels.
"This is the first time a cell cycle protein has been shown to be directly involved in DNA repair," said Siwanon Jirawatnotai, the lead author of the paper.
"If we could come up with a strategy to inhibit cyclin D1, it might be very useful in treating a variety of cancers," he said.
According to the study, the gene for cyclin D1 is the second most-over expressed gene found in human cancers, including breast cancer, colon cancer, lymphoma, melanoma, and prostate cancer.
Cyclin D1's normal function is to temporarily remove a molecular brake, allowing the cell to manufacture more DNA in preparation for cell division.
When cyclin D1 is mutated or is overactivated by external growth signals, the cell may run out of control and proliferate in a malignant fashion.
However, when cancer cells with reduced cyclin D1 protein levels were administered to mice, the resulting tumour proved to be more sensitive to radiation than those grown from cells with over expressed cyclin D1.
The new study strongly suggests that targeting cyclin D1 may increase susceptibility of human cancers to radiation, and this may encourage targeting cyclin D1 even in those cancers whose cells do not depend on cyclin D1 for proliferation.
The study appears in the current issue of Nature.