Tannic Acid Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Prostate Cancer

摘要: Endoplasmic reticulum (ER) stress is an intriguing target with significant clinical importance in chemotherapy. Interference ER functions can lead to the accumulation of unfolded proteins, as detected by transmembrane sensors that instigate protein response (UPR). Therefore, controlling induced UPR via natural compounds could be a novel therapeutic strategy for management prostate cancer. Tannic acid (a naturally occurring polyphenol) was used examine mediated pathway cancer cells. treatment inhibited growth, clonogenic, invasive, and migratory potential demonstrated activation (Protein kinase R-like endoplasmic (PERK) inositol requiring enzyme 1 (IRE1)) altered its regulatory proteins (ATF4, Bip, PDI) expression. affirmed upregulation apoptosis-associated markers (Bak, Bim, cleaved caspase 3, PARP), while downregulation pro-survival (Bcl-2 Bcl-xL). exhibited elevated G1 population, due increase p18INK4C p21WAF1/CIP1 expression, cyclin D1 expression inhibited. Reduction MMP2 MMP9, reinstated E-cadherin signifies anti-metastatic this compound. Altogether, these results demonstrate tannic promote apoptosis pathway, indicating candidate treatment.