New clues to how humble painkiller stifles cancer growth
CANCER RESEARCH UK scientists have shed light on how a common class of painkillers – which includes ibuprofen – may interact with a key protein that fuels the growth of many different types of cancer, according to a study published in the journal Chemical Communications today (Thursday).
Ibuprofen is one of several profens - a particular group of non-steroidal anti-inflammatory drugs (NSAIDs) - being investigated for their ability to prevent cancer.
The University of Bath research team* carried out an analysis of drugs in the same class as ibuprofen and discovered that they are all processed by the body in exactly the same way – through a protein called AMACR, which converts the drug into its active form.
AMACR is overactive in almost all prostate cancers, some bowel cancers and several other types of cancer and is thought to fuel the growth of the disease by boosting the cell’s energy supply.
So understanding how drugs like ibuprofen might alter AMACR activity could help scientists better understand how they are able to block cancer growth.
Lead author Dr Matthew Lloyd, said: “Our study is the first to test other drugs in the same family as ibuprofen systematically and show that they‘re all processed by the same protein in the body. Some early laboratory studies have suggested that high doses of ibuprofen can halt the growth of prostate cancer cells, but the reasons for this aren’t well understood.
“Understanding more about how this protein is acting in cells and what molecules it interacts with could provide important clues to how this process works, hopefully opening up new avenues of research for treating prostate cancer in the future.”
Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “This research is part of an international effort to understand how drugs like ibuprofen could prevent, or slow down, the development of cancer. But there are risks as well as benefits and long term use of these drugs can have side effects, such as bleeding and stomach ulcers. Understanding more about how these drugs work on a molecular level is a crucial step in being able to develop better targeted drugs with fewer side effects in future.”
For media enquiries please contact the Cancer Research UK press office on 020 3469 8300 or, out-of-hours, the duty press officer on 07050 264 059.
Woodman et al., Chiral inversion of 2-arylpropional-CoA esters by human alpha-methyylacyl-CoA racemase 1A (P504S) – a potential mechanism for the anti-cancer effects of ibuprofen (2011), Chemical Communications, DOI: 10.1039/ClCC10763A.
Notes to Editor
*The research, carried out in the Department of Pharmacy & Pharmacology at the University of Bath, was done by a team comprising academic staff, post-doctoral scientists, undergraduate students and a Sixth Form College student. The project was funded by Cancer Research UK and the student projects were funded by the Nuffield Foundation (an Undergraduate Research Bursary and a Science Bursary for Schools and Colleges) and a Bath-Shandong Pharmacy & Pharmacology Scholarship project.