Venom from honeybees has been found to kill aggressive breast cancer cells.

Researchers have tested the effect of bee venom on clinical subtypes of breast cancer, including triple-negative breast cancer, which has limited treatment options.

Using the venom from 312 honeybees and bumblebees in Perth Western Australia, Ireland and England, Dr Ciara Duffy from the Harry Perkins Institute of Medical Research and The University of Western Australia, have found that honeybee venom rapidly destroys triple-negative breast cancer and HER2-enriched breast cancer cells.

“No-one had previously compared the effects of honeybee venom or melittin across all of the different subtypes of breast cancer and normal cells,” Dr Duffy says.

“We tested honeybee venom on normal breast cells, and cells from the clinical subtypes of breast cancer: hormone receptor positive, HER2-enriched, and triple-negative breast cancer.

“We tested a very small, positively charged peptide in honeybee venom called melittin, which we could reproduce synthetically, and found that the synthetic product mirrored the majority of the anti-cancer effects of honeybee venom.

“We found both honeybee venom and melittin significantly, selectively and rapidly reduced the viability of triple-negative breast cancer and HER2-enriched breast cancer cells.

“The venom was extremely potent,” she said.

According to the study, a specific concentration of honeybee venom can induce 100 per cent cancer cell death, while having minimal effects on normal cells.

“We found that melittin can completely destroy cancer cell membranes within 60 minutes,” Dr Duffy said.

Melittin in honeybee venom also had another remarkable effect; within 20 minutes, melittin was able to substantially reduce the chemical messages of cancer cells that are essential to cancer cell growth and cell division.

“We looked at how honeybee venom and melittin affect the cancer signalling pathways, the chemical messages that are fundamental for cancer cell growth and reproduction, and we found that very quickly these signalling pathways were shut down,” Dr Duffy says.

“Melittin modulated the signalling in breast cancer cells by suppressing the activation of the receptor that is commonly overexpressed in triple-negative breast cancer, the epidermal growth factor receptor, and it suppressed the activation of HER2 which is over-expressed in HER2-enriched breast cancer,” she said.

Dr Duffy also tested to see if melittin could be used with existing chemotherapy drugs as it forms pores, or holes, in breast cancer cell membranes, potentially enabling the entry of other treatments into the cancer cell to enhance cell death.

“We found that melittin can be used with small molecules or chemotherapies, such as docetaxel, to treat highly-aggressive types of breast cancer. The combination of melittin and docetaxel was extremely efficient in reducing tumour growth in mice,” she said.

Dr Duffy’s research was conducted as part of her PhD undertaken at Perth’s Harry Perkins Institute of Medical Research at the Cancer Epigenetics laboratory overseen by A/Prof. Pilar Blancafort.

The study is accessible here.