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Tannic Acid Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Prostate Cancer
Prashanth K B Nagesh1, Elham Hatami2, Pallabita Chowdhury3
1Department of Pharmaceutical Sciences and Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN 38163, USA. pbhusett@uthsc.edu.
Abstract:
Endoplasmic reticulum (ER) stress is an intriguing target with significant clinical importance in chemotherapy. Interference with ER functions can lead to the accumulation of unfolded proteins, as detected by transmembrane sensors that instigate the unfolded protein response (UPR). Therefore, controlling induced UPR via ER stress with natural compounds could be a novel therapeutic strategy for the management of prostate cancer. Tannic acid (a naturally occurring polyphenol) was used to examine the ER stress mediated UPR pathway in prostate cancer cells. Tannic acid treatment inhibited the growth, clonogenic, invasive, and migratory potential of prostate cancer cells. Tannic acid demonstrated activation of ER stress response (Protein kinase R-like endoplasmic reticulum kinase (PERK) and inositol requiring enzyme 1 (IRE1)) and altered its regulatory proteins (ATF4, Bip, and PDI) expression. Tannic acid treatment affirmed upregulation of apoptosis-associated markers (Bak, Bim, cleaved caspase 3, and cleaved PARP), while downregulation of pro-survival proteins (Bcl-2 and Bcl-xL). Tannic acid exhibited elevated G₁ population, due to increase in p18INK4C and p21WAF1/CIP1 expression, while cyclin D1 expression was inhibited. Reduction of MMP2 and MMP9, and reinstated E-cadherin signifies the anti-metastatic potential of this compound. Altogether, these results demonstrate that tannic acid can promote apoptosis via the ER stress mediated UPR pathway, indicating a potential candidate for cancer treatment.
Insights
Tannic acid, a natural polyphenol, combats prostate cancer by inducing endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). This natural compound promotes cancer cell apoptosis and inhibits growth, invasion, and metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Endoplasmic reticulum (ER) stress is a critical factor in chemotherapy and cancer progression.
- The unfolded protein response (UPR) is activated by ER stress, making it a potential therapeutic target.
- Natural compounds offer novel strategies for cancer management by modulating cellular stress pathways.
Purpose of the Study:
- To investigate the effects of tannic acid, a natural polyphenol, on ER stress and UPR in prostate cancer cells.
- To determine if tannic acid can be a therapeutic agent for prostate cancer by targeting the ER stress-mediated UPR pathway.
Main Methods:
- Prostate cancer cells were treated with tannic acid.
- Cell growth, clonogenic potential, invasion, and migration were assessed.
- ER stress markers (PERK, IRE1), UPR regulators (ATF4, Bip, PDI), apoptosis markers (Bak, Bim, cleaved caspase 3, cleaved PARP, Bcl-2, Bcl-xL), cell cycle regulators (p18INK4C, p21WAF1/CIP1, cyclin D1), and metastasis markers (MMP2, MMP9, E-cadherin) were analyzed.
Main Results:
- Tannic acid inhibited prostate cancer cell growth, clonogenic potential, invasion, and migration.
- Tannic acid activated ER stress (PERK, IRE1) and modulated UPR regulators (ATF4, Bip, PDI).
- Tannic acid induced apoptosis by upregulating pro-apoptotic markers and downregulating pro-survival proteins, arrested cells in G1 phase, and reduced metastasis markers.
Conclusions:
- Tannic acid effectively suppresses prostate cancer progression by inducing apoptosis through the ER stress-mediated UPR pathway.
- Tannic acid demonstrates significant anti-cancer properties, including anti-proliferative, anti-invasive, and anti-metastatic effects.
- Tannic acid is a promising natural compound for the development of novel prostate cancer therapies.
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