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Sci Rep. 2020 Jan 22;10(1):980. doi: 10.1038/s41598-020-57932-9.

Tannic acid inhibits lipid metabolism and induce ROS in prostate cancer cells.

Author information

1
Department of Microbiology and Immunology, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
2
Department of Pharmaceutical Sciences and Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
3
Tumor Initiation and Maintenance, Sanford-Burnham Medical Research Institute, La Jolla, California, 92037, USA.
4
Department of Pathology, Moores UCSD Cancer Center, and Sanford Consortium for Regenerative Medicine, University of California, San Diego, La Jolla, CA, 92037, USA.
5
Department of Microbiology and Immunology, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA. murali.yallapu@utrgv.edu.
6
Department of Pharmaceutical Sciences and Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, 38163, USA. murali.yallapu@utrgv.edu.

Abstract

Prostate cancer (PCa) cells exploit the aberrant lipid signaling and metabolism as their survival advantage. Also, intracellular storage lipids act as fuel for the PCa proliferation. However, few studies were available that addressed the topic of targeting lipid metabolism in PCa. Here, we assessed the tannic acid (TA) lipid-targeting ability and its capability to induce endoplasmic reticulum (ER) stress by reactive oxygen species (ROS) in PCa cells. TA exhibited dual effects by inhibiting lipogenic signaling and suppression of lipid metabolic pathways. The expression of proteins responsible for lipogenesis was down regulated. The membrane permeability and functionality of PCa were severely affected and caused nuclear disorganization during drug exposure. Finally, these consolidated events shifted the cell's survival balance towards apoptosis. These results suggest that TA distinctly interferes with the lipid signaling and metabolism of PCa cells.

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