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

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.

• Authors: Prashanth K B Nagesh, Pallabita Chowdhury, Elham Hatami, Shashi Jain, Nirnoy Dan, Vivek Kumar Kashyap, Subhash C Chauhan, Meena Jaggi, Murali M Yallapu
• Journal: Scientific reports (Sci Rep) Vol. 10 Issue 1 Pg. 980 (01 22 2020) ISSN: 2045-2322 [Electronic] England
• PMID: 31969643 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)

Chemical References

• Reactive Oxygen Species
• Tannins

Topics

• Apoptosis (drug effects)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cell Survival (drug effects)
• Endoplasmic Reticulum Stress (drug effects)
• Humans
• Lipid Metabolism (drug effects)
• Male
• Prostate (drug effects, metabolism)
• Prostatic Neoplasms (metabolism)
• Reactive Oxygen Species (metabolism)
• Signal Transduction (drug effects)
• Tannins (pharmacology)