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Interrogating metabolic cross-talk in the tumour-bone microenvironment, new research from the Edwards Group shows how the pentose phosphate pathway contributes to prostate cancer bone metastasis.

Prostate cancer is the second leading cause of cancer-related death in men. While overall five-year survival rates for prostate cancer are 97.8%, in metastatic disease this falls to only 30%.

Once prostate cancer metastasises to bone, treatment options are limited and the malignancy becomes incurable. Prostate cancer cells are exquisitely dependent upon cellular interactions within the bone microenvironment to drive both tumour growth and survival and the development of the associated bone disease.

Research from Professor Claire Edwards’ team at the Botnar Research Centre, and published in Science Advances, identifies a new mechanism by which the bone microenvironment alters the energy requirements of prostate cancer cells to support disease progression. 

'The importance of cellular cross-talk within the tumour-bone microenvironment has long been recognised,' said Professor Edwards. 'In this study we show how bone cells alter the metabolic activity of prostate cancer cells.'

The first author of the study, Dr Jessica Whitburn, said: 'Through a collaboration with Professor Tomoyoshi Soga, Keio University, we used metabolomic profiling to identify changes in the pentose phosphate pathway. Genetic and pharmacologic manipulation of G6PD, the rate-limiting enzyme of this pathway, had a significant impact on prostate cancer cell growth, migration, metabolism and chemosensitivity. 

'The ability of cancer cells to reprogramme their cellular metabolism has recently been recognised as an additional hallmark of cancer. By understanding how the bone microenvironment drives the metabolic plasticity of prostate cancer cells, we reveal new mechanisms underlying disease pathogenesis and new metabolic targets for the treatment of prostate cancer bone metastasis.'

 

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