Abstract
Aims: Triple-negative breast cancer patients are commonly treated with combination chemotherapy. Nonetheless, outcomes remain substandard with relapses being of a frequent occurrence. Among the several mechanisms that result in treatment failure, multidrug resistance, which is mediated by ATP-binding cassette proteins, is the most common. Regardless of the substantial studies conducted on the heterogeneity of cancer types, only a few assays can distinguish the variability in multidrug resistance activity between individual cells. We aim to develop a single-cell assay to study this.Methods: This experiment utilized a microfluidic chip to measure the drug accumulation in single breast cancer cells in order to understand the inhibition of drug efflux properties.Results: Selection of single cells, loading of drugs, and fluorescence measurement for intracellular drug accumulation were all conducted on a microfluidic chip. As a result, measurements of the accumulation of chemotherapeutic drugs (e.g., daunorubicin and paclitaxel) in single cells in the presence and absence of cyclosporine A were conducted. Parameters such as initial drug accumulation, signal saturation time, and fold-increase of drug with and without the presence cyclosporine A were also tested.Conclusion: The results display that drug accumulation in a single-cell greatly enhanced over its same-cell control because of inhibition by cyclosporine A. Furthermore, this experiment may provide a platform for future liquid biopsy studies to characterize the multidrug resistance activity at a single-cell level.
Highlights
Despite the recent progression in cancer treatments, breast cancer is still the most common female malignancy worldwide[1]
Selection of single cells, loading of drugs, and fluorescence measurement for intracellular drug accumulation were all conducted on a microfluidic chip
The results display that drug accumulation in a single-cell greatly enhanced over its same-cell control because of inhibition by cyclosporine A
Summary
Despite the recent progression in cancer treatments, breast cancer is still the most common female malignancy worldwide[1]. Malignant epithelial cells can be unresponsive or hyperactive to the hormones, estrogen, and progesterone[2], resulting in uncontrolled cellular growth and proliferation. Triple-negative breast cancer (TNBC), which lacks expression of the estrogen, progesterone, and HER2 receptor, is often a basal-like breast cancer capable of growing high-grade aggressive tumors that can spread quickly. Neither hormonal therapy nor targeted therapy is offered for triple-negative or basallike breast cancers[2]. While novel immunotherapies have shown great promise in several cancers, in TNBC, only very tentative initial trials have been completed. It appears that the best option for those approaches to be effective will be as part of a mix of therapeutic approaches that includes chemotherapy and targeted therapies
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