Whether metastases develop is determined by the interactions between various factors, but it is not always clear how these factors contribute to the mechanisms that drive this multi-component process. Cancer cells that are capable of spreading throughout the body often originate and can thrive in hypoxic (low oxygen) environments, and hypoxic tumours are clinically linked to poor patient outcome. Previous investigations of hypoxic tumour physiology established a link between hypoxia and elevated LOX expression. Building on these findings, Erler and colleagues analysed breast, head and neck cancer studies, and found that hypoxic breast cancer cells had elevated levels of LOX expression, with a lower probability of survival for those patients whose tumour cells expressed higher levels of LOX.
To investigate the therapeutic potential of blocking LOX activity, the authors implanted mice with tumours grown from human breast cancer cells engineered to produce significantly less LOX than normal cells. Metastatic cancer cells were detected in the lungs and liver of control animals that received wildtype tumours. However, mice that received modified tumours expressing lower levels of LOX had fewer metastatic cells in their lungs and none in their liver. Metastasis was completely abolished by giving the control mice β-aminoproprionitrile, an irreversible LOX inhibitor. This response was also achieved using an antibody against LOX.
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