Background The MYC oncogene is one of the most frequently altered driver genes in
cancer. MYC is thus a potential target for
cancer treatment as well as a
biomarker for the disease. However, as a target for treatment, MYC has traditionally been regarded as "undruggable" or difficult to target. We set out to evaluate the efficacy of a novel MYC inhibitor known as
MYCMI-6, which acts by preventing MYC from interacting with its cognate partner MAX. Methods
MYCMI-6 response was assessed in a panel of
breast cancer cell lines using MTT assays and flow cytometry. MYC gene amplification,
mRNA and
protein expression was analysed using the TCGA and METABRIC databases. Results
MYCMI-6 inhibited cell growth in
breast cancer cell lines with IC50 values varying form 0.3 μM to >10 μM. Consistent with its ability to decrease cell growth,
MYCMI-6 was found to induce apoptosis in two cell lines in which growth was inhibited but not in two cell lines that were resistant to growth inhibition. Across all breast
cancers, MYC was found to be amplified in 15.3% of cases in the TCGA database and 26% in the METABRIC database. Following classification of the breast
cancers by their molecular subtypes, MYC was most frequently amplified and exhibited highest expression at both
mRNA and
protein level in the basal subtype. Conclusions Based on these findings, we conclude that for patients with
breast cancer, anti-MYC
therapy is likely to be most efficacious in patients with the basal subtype.