Scientists finds commonly prescribed painkiller may slow growth rate of cancer

One of the most widely prescribed pain and anti-inflammation drug may also slow the growth rate of cancer, a new study has found. The study focused on the effects of celecoxib or Celebrex. It targets an enzyme called “cyclooxygenase-2” (COX-2), which is linked to pain and inflammation, researchers said. This enzyme is also critical in the creation of prostaglandins, compounds that act like hormones and play a role in promoting tumour growth, they said.

COX-2 expression is typically low in normal tissue, but high in multiple types of cancers, researchers said. “We were actually interested in determining what a particular signalling pathway does in cancer,” said Joseph Kissil from The Scripps Research Institute (TSRI) in the US.

“In the process, we found that it activates genes that promote survival of tumour cells and that they do so by turning on enzymes involved in inflammation, including COX2, which anti-inflammatory drugs like Celebrex inhibit,” said Kissil.

Researchers conducted animal studies tracking the effects of celecoxib on the growth of cancer cells from a tumour type known as neurofibromatosis type II (NF2).

In humans, NF2 is a relatively rare inherited form of cancer caused by mutations in the anti-tumour gene NF2, which leads to benign tumours of the auditory nerve, researchers said.

Animals received a daily dose of the drug, and tumour growth was followed by imaging. Analysis of the results showed a significantly slower tumour growth rate in celecoxib-treated models than in controls, they said.

Using various approaches, the study also showed that a signalling cascade known as the Hippo-YAP pathway is involved in these results and that the protein YAP is required for the proliferation and survival of NF2 cells and tumour formation.

“Our study shows that COX2 inhibitors do have an effect on the tumour cells. They also have an impact on inflammatory responses that play a role in tumour growth,” said William Guerrant from TSRI. “It is possible that in other cancers these effects might actually be stronger because of the drug’s impact on inflammation,” he said.