In solid tumor, there is a region where oxygen supply is insufficient. Under this hypoxic condition, cancer cells became more resistant than normal cells. In this study, we found that one of the aminoglycoside antibiotics, geneticin, made a human breast cancer cell, MCF-7, even more resistant to hypoxia.

On normoxic (21% O₂) condition, MCF-7 cells (1.5×10⁶ cells/60 mm culture dish) were grown in low glucose (1 g/l) MEM (with 10% FBS) supplemented with 0, 1, 10, 100, and 1000µg/dl geneticin, respectively, for one day. Then, the cells were transferred to hypoxic (1% O₂) incubator and grown for 3 days. We examined the viability of cells, the concentration of glucose and lactate and DNA fragmentation assay in each groups.

When the cells were grown in low glucose medium under hypoxia (1% O₂), all the cells became dead after 2 days of culture in the absence of geneticin whereas the cells still survived even after 3 days of culture in the presence of geneticin (10µg/ml). In the presence of geneticin, the cells survived despite of consumption of all glucose in the medium, whereas the cells became dead once all glucose was consumed in the absence of geneticin. In this case, geneticin made cells survive by suppressing apoptosis, which was proved by DNA fragmentation assay.

The results might have some implications in treating solid tumor; if cancer patients should be treated for infection with antibiotics, aminoglycoside antibiotics can aggravate the patient's condition by making cancer cells more resistant to hypoxia. Therefore, the results strongly suggest that we should be careful in choosing antibiotics when they are used for cancer patients.