The study found treatment with auranofin reduced survival of ovarian cancer cells with faulty BRCA1 genes.
The study - by researchers at the University of Plymouth in the UK, working with the nearby Plymouth Oncology Centre at Derriford Hospital - is published in the journal Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis.
BRCA1 is a protein that repairs DNA. If there is a mutation in the gene that codes for it, it can lead to an insufficient amount of the protein, which results in DNA damage not being repaired. This increases the chance that affected cells will develop further gene alterations and become cancerous.
Previous studies have also suggested that breast and ovarian cancers that have BRCA1 mutations may also be more sensitive to drugs that damage DNA - the cancer cells may more easily succumb to the drugs.
Auranofin is currently undergoing trials for repurposing to treat recurrent epithelial ovarian cancer, which accounts for around 90% of diagnosed ovarian cancers.
Using already-available drugs such as auranofin to treat cancer is highly promising because their effects on the body are well documented, notes corresponding author Awadhesh Jha, professor of toxicology and associate head (research) in Plymouth's School of Biological Sciences.
Survival of BRCA1-depleted cancer cells reduced by up to 37%
Prof. Jha and colleagues investigated the effect of auranofin on ovarian cancer cells grown in the lab.
They found that lack of BRCA1 protein rendered the cells more vulnerable to auranofin, compared with ovarian cancer cells with normal versions of the gene.
Moreover, the lab tests showed that BRCA1-depleted ovarian cancer cells treated with auranofin suffered more irreparable damage - in the form of lethal DNA double-strand breaks.
For the study, the team tested auranofin on two types of ovarian cancer cell - OVCAR5 and SKOV3 - with BRCA1 expression levels depleted and compared the results with a control set.
They found that even before BRCA1 depletion, the SKOV3 cells were already relatively sensitive to auranofin, and with BRCA1 depletion, the survival of the cancer cells was reduced by up to 37%, with an auranofin concentration of 1 part per million.
Similarly, treating BCRA1-deplected OVCAR5 cells with auranofin also reduced cancer cell survival, compared with non-depleted cells.
Prof. Jha sums up the implication of the study:
"It suggests that auranofin has the potential to be considered for future clinical studies to treat such ovarian cancers and this could serve as the springboard to use other available drugs which are not used as chemotherapeutic drugs."
The new study follows an earlier Medical News Today report from August 2015 about a potential gene therapy for ovarian cancer that recurs after chemotherapy. The researchers found that gene therapy - consisting of a single injection of a modified sexual development protein - stopped the growth of chemotherapy-resistant ovarian cancer tumors in mice. The recurrence of ovarian cancer after chemotherapy happens in the majority of cases and is invariably fatal.