22 Jan 2014

Prostate Cancer UK funded scientists at Newcastle University have found a new trick that prostate cancer cells use to escape from the body’s usual methods of controlling cell growth. This may help to explain why some treatments don’t work as well as expected.

Researchers in Professor David Elliot’s lab have discovered that when prostate cancer cells come into contact with testosterone (the male hormone that turns on the androgen receptor and drives prostate cancer cell growth), a gene called TSC2 starts behaving unusually.

TSC2: Flicking the switch

In normal cells, TSC2 stops cells growing, which prevents cancer developing.  But when prostate cancer cells are exposed to testosterone, a different form of TSC2 is turned on instead.  The really surprising thing about this is that the ‘alternative’ form of TSC2 works in a completely opposite way to normal!

Same gene, different job

We can best explain how this works by thinking of a gene like a sentence. When we read a sentence with the words and punctuation in the correct places, it has a certain meaning.  If we now rearrange, add or delete some words, or change the punctuation, the meaning of the sentence changes. The same thing happens to genes. When a gene like TSC2 is ‘read’ in one way, it stops tumour growth.  If we now change the ‘punctuation’ of the gene so that we only read (or express) a shorter part of TSC2, which is what happens in prostate cancer cells, it works in a completely opposite way and starts to encourage prostate cancer cell growth instead of stopping it.

Implications for the future

This surprising discovery might turn out to have important clinical implications, because it means that cancer cells have a previously unknown mechanism for evading the body’s control systems, which might also mean a new way for cancer cells to become resistant to therapy. This might be important to know when designing new drugs in the future, to help avoid this pitfall.

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