Oncogenes are genes that drive so-called 'transformed cells' to excess proliferation when they are deregulated and overexpressed. The expression of oncogenes sensitizes transformed cells to drugs (as compared with normal cells) and such drugs can thus be used to prevent cellular proliferation and hence be used for cancer therapy. Understanding the rationale behind the different sensitivity to anti-cancer drugs of transformed cells versus normal cells may provide new strategies to selectively destroy tumour cells.
There are two possible explanations to account for the differential sensitivity to anti-cancer drugs of transformed cells versus normal cells: either the expression of oncogenes 'actively' predispose cells to apoptosis (cell death), or normal cells are intrinsically protected from apoptosis and oncogenes somehow overcome this protection. Yuri Lazebnik and his colleagues at Cold Spring Harbor Laboratory, NY, now provide evidence in favour of the latter hypothesis on pages 859-862 of the November issue of Nature Cell Biology. They tackle the problem by generating a fusion between transformed cells expressing the adenoviral E1A oncogene and normal cells. If it is transformed cells that 'actively' drive the cells towards death, then the product of the fusion (the heterocaryon) is expected to be sensitive to anti-cancer drugs. If, on the contrary, it is normal cells that provide an 'active' resistance cue, then the heterocaryon would be resistant to anti-cancer drugs. It turns out that the heterocaryon is indeed resistant to anti-cancer drugs. The authors checked that this was not due to trivial reasons such as dilution of the E1A oncogene. Thus, normal cells are intrinsically resistant to anti-cancer drugs and oncogenes somehow neutralize this protection pathway. Once we find out how this is achieved, which is what Yuri Lazebnik and his collaborators are currently working on, advantage could be taken of this specific 'weakness' of transformed cells in anti-cancer treatments.
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