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Sulfasalazine attenuates tamoxifen-induced toxicity in human retinal pigment epithelial cells
Narae Hwang1 (Narae Hwang), Su Wol Chung 2,* (Su Wol Chung)
1Biological Sciences, University of Ulsan
Tamoxifen, a nonsteroidal estrogen receptor (ER) antagonist, is used routinely as a chemotherapeutic agent for ER-positive breast cancer. However, it is also known to cause side effects, including retinotoxicity. The retinal pigment epithelium (RPE) has been recognized as the primary target of tamoxifen-induced retinotoxicity. The RPE is essential physiological roles in the normal functioning of the retina. Nonetheless, potential therapeutic agents to prevent tamoxifen-induced retinotoxicity in breast cancer patients have not been investigated. Here, we evaluated the action mechanisms of sulfasalazine against tamoxifen-induced RPE cell death. Tamoxifen induced reactive oxygen species (ROS)-mediated autophagic cell death and caspase-1-mediated pyroptosis in RPE cells. However, sulfasalazine reduced tamoxifen-induced total ROS and ROS-mediated autophagic RPE cell death. Moreover, mRNA levels of tamoxifen-induced pyroptosis-related genes, IL-1モ, NLRP3, and procaspase-1, were also decreased in the presence of sulfasalazine in RPE cells. Furthermore, the mRNA levels of tamoxifen-induced AMD-related genes, such as complement factor I (CFI), complement factor H (CFH), apolipoprotein E (APOE), apolipoprotein J (APOJ), toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4), were downregulated in RPE cells. Taken together, these data provide novel insight into the therapeutic effects of sulfasalazine against tamoxifen-induced RPE cell death.
Abstract, Accepted Manuscript(in press) [Submitted on February 20, 2020, Accepted on April 10, 2020]
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