Source: University of East Anglia
Summary: According to a new research, it is found that cancer therapies that cut off blood supply to a tumour could be more effective in combination with existing chemotherapeutic drugs.
Anti-angiogenic drugs stop tumours from growing their own blood vessels, and this, in turn, can slow the growth of cancer, or shrink it. Targeting angiogenesis is therefore seen as crucial in many anti-cancer strategies. However many anti-angiogenetic therapies target proteins that help the functioning of a patient’s normal blood supply and this can lead to nasty side effects including haemorrhage, strokes, high blood pressure, and fatigue. Researchers from the University of East Anglia revealed that tumour growth is better-reduced in mice when the expression of a particular protein called Beta3-integrin is targeted in combination with drugs that are already used in cancer patients. The study findings were published in the journal EMBO reports.
The research team has long looked at Beta3-integrin as a better anti-angiogenic target because the protein is not expressed in normal blood vessels, but is expressed in tumour blood vessels. This reduces the potential for unwanted side effects. Now the team has shown that targeting Beta3-integrin in combination with microtubule-targeting agents, which are widely used in cancer patients, works better than targeting Beta3-integrin alone. Microtubules are protein structures in cells that help them move and divide. It is hoped that the findings could help fine-tune treatment for cancer patients and revitalize an interest in the use of microtubule-targeting agents (MTAs) which are commonly used as chemotherapies in cancer patients.
Lead researcher Dr. Stephen Robinson said, “We found that targeting the protein Beta3-integrin in combination with the use of microtubule-targeting agents (MTAs) could be a good way to stop tumours recruiting a blood supply to grow.”
More Information: Samuel J Atkinson et al, “The β3‐integrin endothelial adhesome regulates microtubule‐dependent cell migration”, EMBO reports (2018). DOI: 10.15252/embr.201744578