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Sulforaphane Protects Cardiac Cells from Doxorubicin-toxicity without Inhibiting Anti-cancer Activity

Graduate #5
Discipline: Biological Sciences
Subcategory: Cancer Research

Jaz'mon Moore - Jackson State University
Co-Author(s): Mecit Kaplan, Vetriselvan Manavalan, and Sharda P. Singh, Department of Pharmacology and Toxicology, UAMS Clement Yedjou, Department of Biology, Jackson State University



Background: Cardiomyopathy due to oxidative/electrophilic stress often occurs after doxorubicin (DOX) chemotherapy of major malignancies, and may predispose to heart disease. Sulforaphane (SFN), a phytochemical, is known to activate the transcription factor Nrf2 and induce defense mechanisms in normal cells. SFN also inhibits cancer cells seemingly through Nrf2 independent mechanisms. Our studies show that sulforaphane (SFN) protects cardiomyocytes from DOX toxicity by activating Nrf2 without compromising the ability of DOX to kill cancer cells. Therefore, sulforaphane could be a valuable adjuvant in DOX-therapy. Methods: To test whether SFN concentrations that protect cardiac cells compromise the ability of DOX to kill cancer cells in vitro, we assayed cell survival and Nrf2 activity in cancer and cardiac cells. H9c2 (cardiac cell line) and 13762 MAT BIII (breast cancer line) were treated for 24h with either DMSO vehicle, 2.5 µM SFN, 5 µg/ml DOX, or DOX + 2.5 µM SFN. Survival was assayed by the Calcein Blue, Acetoxymethyl (AM) assay. Active Nrf2 was measured in cardiac and cancer cells after SFN (2.5 µM), DOX (5 µg/ml) or SFN +DOX treatment for 24h, control cells received DMSO. Results: SFN enhances survival in DOX-treated cardiac H9c2 cells but selectively maintains or enhances DOX-killing of breast cancer cells. SFN enhanced nuclear Nrf2 activity in cardiac H9c2 cells even in the presence of DOX. We detected high basal levels of nuclear Nrf2 activity in the cancer cells compared to cardiac cells and SFN treatment did not alter Nrf2 activity in cancer cells. Discussion & Conclusions: Our initial results suggest that DOX and SFN act synergistically in cancer cell kill, which may improve therapeutic index of DOX in cancer-therapy. These results imply that Nrf2 activation in cardiac cells, with low Nrf2 activity, is induced by SFN treatment and, unlike in cancer cells, SFN confers cardiac protection from DOX toxicity. Invasive cancer cells are inhibited by DOX chemotherapy but are not protected by SFN treatment, perhaps because Nrf2 is not activated by SFN in those cells. Taken together we demonstrated preclinical proof of principle for SFN/DOX co-therapy for breast cancer.

Funder Acknowledgement(s): Sharda Singh- Advisor, Mecit Kaplan, SURP NIH- Grant 5R25HL108825, LSAMP Kristen Sterba, VA Medical Center, UAMS

Faculty Advisor: Sharda P. Singh, SinghShardaP@uams.edu

Role: Treated the H9c2 cells with DOX and SFN.

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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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