Background: Glucocorticoids are commonly co-administered with chemotherapy to prevent drug-inducedallergic reactions, nausea, and vomiting, and have anti-tumor functions clinically; however, the distinct effectsof GC on subtypes of tumor cells, especially in breast cancer cells, are still not well understood. In this study,we aimed to clarify the effect of GC on subtypes of T47D breast cancer cells by focusing on apoptosis, cellorganization and migration, and underluing molecular mechanisms. Materials and
Methods: The cell scratchtest was performed to observe the cell migration rate in T47D cells treated with dexamethasone (Dex). Hoechstand MTT assays were conducted to detect cell survival and rhodamine-labeled phalloidin staining to observecytoskeleton dynamics. Related factors in the AKT/mTOR pathway were determined by Western blotting.
Results:Dex treatment could effectively inhibit T47D breast cancer cell migration with disruption of the cytoskeletaldynamic organization. Moreover, the effect of Dex on cell migration and cytoskeleton may be mediated by AKT/mTOR/RhoA pathway. Although Dex inhibited T47D cell migration, it alone may not induce cell apoptosis inT47D cells.
Conclusions: Dex in T47D human breast cancer cells could effectively inhibit cell migration bydisrupting the cytoskeletal dynamic organization, which may be mediated by the AKT/mTOR/RhoA pathway.Our work suggests that glucocorticoid/Dex clinical use may prove helpful for the treatment of breast cancermetastasis.