Repurposing beta blockers for the treatment of cancer

Beta blockers have long been used to treat a number of diseases, such as high blood pressure, heart failure, glaucoma, and migraines. These drugs work by affecting two stress response hormones, epinephrine (EPI)(also known as adrenaline, adrenalin) and norepinerphine (NE). EPI and NE are stress hormones involved in the body’s “fight or flight” response to psychological stressors. These hormones bind to their receptors, called adrenoceptors, and transmit signals into the cell that alter its behavior (i.e., to begin growing and dividing). Any cell bearing these receptors on its surface will receive the signal. As their name implies, beta blockers prevent EPI and NE from binding to the beta type of adrenoceptors on the cell, thus stopping further signaling to the inside of the cell.

Beta blockers and cancer

An increasing number of studies have shown a possible benefit to using beta blockers, a common treatment for high blood pressure, for the treatment of several types of cancers.

One study demonstrated that cancer growth was slowed in mice that had been given pronanolol, a common beta blocker, compared to untreated mice. A very recent, retrospective study showed that patients with triple-negative breast cancer, a particularly aggressive form of cancer, were significantly less likely to experience recurrence of their cancers if they were also receiving beta blockers. Still other studies have shown that beta blockers may reduce the growth of breast cancer, prostate cancer, and malignant melanoma.

So why might beta blockers be able to treat cancer?

One current hypothesis in the scientific community is that NE may contribute directly to progression of some types of cancers. The receptors that beta blockers target are found in nearly all types of body tissues, as well as in many types of cancers. Additionally, research has shown that increased levels of NE tended to promote cancer progression in rats.

Psychological stress and genetics have also been linked to cancer incidence. For example, chronic stress has been shown to increase ovarian tumor growth in mice. The stress response hormones, NE and EPI, as well as another well-known stress hormone, cortisol, have been specifically linked to the correlation between stress and cancer risk. From the genetic standpoint, the baseline levels of NE and EPI vary from person to person. If a person’s baseline levels of these hormones are high, that may predispose them to cancer. If a person with a higher baseline of NE or EPI is exposed to higher levels of stress, they may be especially susceptible to developing cancer.

The bottom line:

If stress hormones such as NE and EPI are linked to cancer risk, then drugs that have been used to block these hormones have the potential to be repurposed for the treatment of cancer. One benefit of such a move is that beta blockers are already approved for the treatment of other diseases; they are a relatively safe category of drugs already in use. Of course, more basic and preclinical research will be necessary to realize the full potential of these findings. Meanwhile, experts recommend for patients to discuss with their physicians about the benefit of beta blockers, particularly if they have cancer and hypertension.

Paul Zhang, M.D., Ph.D.

Institute of Integrative BioOncology

Houston, Texas