Role of TRAP1 Protein in the Development and Progression of Glioblastoma

Glioblastoma is recognized as the most aggressive type of primary brain tumor. Despite recent advances in understanding the molecular mechanisms involved in the biology of glioblastoma, patient survival rates remain disappointing, primarily due to the lack of effective treatment options. Tumor necrosis factor receptor-associated protein 1 (TRAP1), a member of the heat shock protein 90 (Hsp90) family, refers to a protein predominantly localized in the mitochondria that regulates both cellular metabolic reprogramming and mitochondrial apoptosis. This protein is highly expressed in several types of tumors, including colorectal cancer, breast cancer, prostate cancer, and lung cancer, and is often associated with drug resistance. However, TRAP1 is also downregulated in certain cancers such as ovarian cancer, bladder cancer, and renal cancer, where its lower expression correlates with poorer prognoses and chemoresistance. The role of TRAP1 lies in enhancing or suppressing oxidative phosphorylation, with the impact of such regulation on tumor development and progression being a matter of ongoing debate. These observations prompt further investigation into the mechanisms responsible for the dual role of TRAP1 as both an oncogene and a tumor suppressor in specific types of tumors, particularly glioblastoma. The present study reviews the role of TRAP1 in the development and progression of glioblastoma and discusses the potential of targeting TRAP1 as a novel therapeutic approach against tumors.