Dieckol prevents prostate cancer cell proliferation by transcriptionally attenuating JAK/STAT3 signaling pathway.

Abstract

This study delved at how the natural substance dieckol (DCL) prevents prostate cancerous cells from proliferating and migrating by blocking the JAK/STAT3 signaling pathway in PC-3 cells. For numerous tests, the cells were treated to DCL at a range of concentrations (0-20 μM) for 24 h. DCL mediated cytotoxicity was analyzed by MTT assay. To evaluate ROS, DCFH-DA staining was employed. Dual (AO/EtBr) staining was utilized to examine apoptotic changes, and MMP levels in PC-3 cells were examined using the appropriate fluorescent staining assays. By using flow cytometry and western blotting, the protein expressions of cell survival, cell cycle, proliferation, and apoptosis were assessed. The results showed that DCL significantly cytotoxically affects PC-3, and the IC50 was discovered to be 12 μM for 24 h exposure. Furthermore, after DCL treatment in PC-3, considerable ROS generation and increased apoptotic signals were detected. STAT3, JAK1, PCNA, and cyclins D1 and E1 are all suppressed by DCL in PC-3. In addition, DCL therapy in PC-3 dramatically increased pro-apoptotic proteins such Bax, caspase-3, and cytochrome C. Therefore, DCL has been regarded as a chemotherapeutic agent because to its ability to decrease the expression of proteins that control cell proliferation, including STAT3, JAK1, PCNA, and cyclins D1 and E1.