Modification of breast cancer cells’ sensitivity to metformin during co-cultivation with Bifidobacterium animalis

Glucose metabolism (GM) disturbances are well-known risk factors for the development of breast cancer (BC). The GM regulator metformin is used as an adjunctive therapy for BC. Another potent modulator of GM in BC cells is the microbiota, particularly bifidobacteria. The combined action of these factors may lead to unpredictable effects on the sensitivity of malignant cells to antitumor agents. Aim. To investigate the effect of Bifidobacterium animalis on the sensitivity of BC cells to the antiproliferative effects of metformin. Materials and Methods. The impact of B. animalis on GM in BC cells was determined by biochemical methods (glucose consumption and lactate production rate, intracellular lactate dehydrogenase activity). Cell viability was evaluated using the trypan blue exclusion test. Results. Co-cultivation of BC cells with B. animalis leads to enhanced glycolysis in malignant cells. These metabolic phenotype changes are accompanied by alterations in the sensitivity of BC cells to metformin. Only in MCF-7 cells treated with B. animalis was a significant enhancement of the antitumor effects of metformin observed compared to cells incubated with either metformin or B. animalis alone. Conclusions. Exposure of MCF-7 cells to B. animalis increases their sensitivity to the antiproliferative effects of metformin, which is a result of GM reprogramming.