Department of Microbiology and Immunology, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Department of Pharmaceutical Sciences and Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Sci Rep. 2020 Jan 22;10(1):980. doi: 10.1038/s41598-020-57932-9.
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.
前列腺癌 (PCa) 细胞利用异常的脂质信号和代谢作为其生存优势。此外,细胞内储存的脂质可作为 PCa 增殖的燃料。然而,很少有研究涉及靶向 PCa 中脂质代谢的问题。在这里,我们评估了单宁酸 (TA) 通过活性氧 (ROS) 靶向脂质的能力及其诱导内质网 (ER) 应激的能力在 PCa 细胞中。TA 通过抑制生脂信号和抑制脂质代谢途径表现出双重作用。负责生脂的蛋白质的表达下调。药物暴露时,细胞膜的通透性和 PCa 的功能受到严重影响,并导致核组织紊乱。最后,这些综合事件将细胞的生存平衡转向凋亡。这些结果表明,TA 明显干扰了 PCa 细胞的脂质信号和代谢。