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Oxidative Stress in MCF-7 and MCF-7/CD44s Breast Cancer Cells

Undergraduate #24
Discipline: Biological Sciences
Subcategory: Cancer Research

Amina Gauff - Delaware State University
Co-Author(s): Alexis Shelton, Delaware State University, DE



The cell membrane hyaluronan receptor and signal transducer CD44 is involved in cellular responses against oxidative stress in breast cancer cells. Nrf2, a transcription factor and master regulator involved in protecting cells via the antioxidant response element (ARE) is normally activated in response to oxidative stress insults. Because the expression of Nrf2 is potentially regulated by CD44 via its intracytoplasmic domain (i.e., CD44-ICD), we hypothesize that CD44 in breast cancer cells influences the Nrf2-dependent response against oxidative stress. To test this hypothesis, we treated MCF-7 (CD44 negative) and MCF-7/CD44s cells (an MCF-7-derived CD44s stable transfectant cell line) with hydrogen peroxide (H2O2), which induces oxidative stress. The cell viability was assessed by MTS assay. MCF-7/CD44s cells appeared to be more sensitive than MCF-7 cells. Consistent with that result, an ARE-mediated luciferase reporter vector assay showed lower luciferase activity in MCF-7 cells compared to in MCF-7/CD44s cells. These findings suggest that the expression of CD44s in MCF-7 cells makes them more sensitive to H2O2-mediated oxidative stress.

Not Submitted

Funder Acknowledgement(s): This study was supported in part by a Delaware Economic Development Office (DEDO) Research Grant (K.M.), an NSF HBCU UP Research Initiation Award (K.M.) and an NNSA grant (H.Boukari).

Faculty Advisor: Karl Miletti-Gonzalez, kmiletti@desu.edu

Role: Analysis of H2O2-treated cells viability (MTS).

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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