17-AAG Induces Endoplasmic Reticulum Stress-mediated Apoptosis in Breast Cancer Cells, Possibly Through PERK/eIF2α Up-regulation
This study explored how 17-AAG, a drug that blocks the heat shock protein HSP90, might work to kill breast cancer cells. Using a pharmacology network and gene analysis, researchers identified that HSP90 could be a key connection between 17-AAG and genes linked to breast cancer. Lab tests showed that 17-AAG slowed down cell growth and triggered cell death in breast cancer cells. The drug also raised cellular oxidant levels and increased stress-related proteins, PERK and eIF2α. Further tests showed that this protein stress led to DNA damage, suggesting a breakdown in cell function. The study highlights HSP90 as a potential treatment target for breast cancer, with 17-AAG showing promise as a therapy that disrupts cellular stress pathways to induce cancer cell death.
![](https://pathobiology.sc.mahidol.ac.th/wp-content/uploads/2025/01/2024-17-AAG.png)