Mechanism and Role of Endoplasmic Reticulum Stress in Osteosarcoma

Osteosarcoma is the most common malignant bone tumor, often occurring in children and adolescents. The etiology of most patients is unclear, and the current conventional treatment methods are chemotherapy, radiotherapy, and surgical resection. However, the sensitivity of osteosarcoma to radiotherapy and chemotherapy is low, and the prognosis is poor. The development of new and useful treatment strategies for improving patient survival is an urgent need. It has been found that endoplasmic reticulum (ER) stress (ERS) affects tumor angiogenesis, invasion, etc. By summarizing the literature related to osteosarcoma and ERS, we found that the unfolded protein response (UPR) pathway activated by ERS has a regulatory role in osteosarcoma proliferation, apoptosis, and chemoresistance. In osteosarcoma, the UPR pathway plays an important role by crosstalk with autophagy, oxidative stress, and other pathways. Overall, this article focuses on the relationship between ERS and osteosarcoma and reviews the potential of drugs or gene targets associated with ERS for the treatment of osteosarcoma.

Automated summary

Osteosarcoma, the most common malignant bone tumor, has a poor prognosis and low sensitivity to current treatment methods. Endoplasmic reticulum stress (ERS) has been found to play a role in regulating osteosarcoma proliferation, apoptosis, and chemoresistance through the unfolded protein response (UPR) pathway. Further research on the relationship between ERS and osteosarcoma could lead to the development of more effective treatment strategies.