Long Bao1, Xiang Li2, Zhixiong Lin1. 1. Department of Neurosurgery, Beijing Sanbo Brain Hospital, Capital Medical University , Beijing , China. 2. Department of Pediatrics, The First Affiliated Hospital of Jinzhou Medical University , Jinzhou , Liaoning , China.
Abstract
Objective: PTEN has been acknowledged as an anticancer factor in the progression of glioblastoma. Mitochondrial division has been found to be associated with cancer cell death. Objective: The aim of our study is to explore whether PTEN attenuates the development of glioblastoma by modulating mitochondrial division. Materials and methods: PTEN adenovirus was used to overexpress PTEN in U87 cells. Mitochondrial function was detected via western blot and immunofluorescence. Pathway blocker was used to inhibit the Akt activation. Results: The results of our study demonstrated that PTEN overexpression reduced cell viability by increasing cell apoptosis. At the molecular level, PTEN overexpression activated mitochondrial apoptosis by mediating mitochondrial dysfunction. Furthermore, we found that Drp1-related mitochondrial division was required for PTEN-mediated mitochondrial dysfunction and cell death. Finally, we found that PTEN modulated Drp1-related mitochondrial division via the Akt pathway; inactivation of Akt induced cell death, and mitochondrial damage, similar to the results obtained via PTEN overexpression. Conclusions: Taken together, our results clarify that the anticancer mechanism of PTEN in glioblastoma is dependent on the activation of Drp1-related mitochondrial division via Akt pathway modulation. This finding might provide new insight into the tumor-suppressive role played by PTEN in glioblastoma.
Objective: PTEN has been acknowledged as an anticancer factor in the progression of glioblastoma. Mitochondrial division has been found to be associated with cancer cell death. Objective: The aim of our study is to explore whether PTEN attenuates the development of glioblastoma by modulating mitochondrial division. Materials and methods: PTENadenovirus was used to overexpress PTEN in U87 cells. Mitochondrial function was detected via western blot and immunofluorescence. Pathway blocker was used to inhibit the Akt activation. Results: The results of our study demonstrated that PTEN overexpression reduced cell viability by increasing cell apoptosis. At the molecular level, PTEN overexpression activated mitochondrial apoptosis by mediating mitochondrial dysfunction. Furthermore, we found that Drp1-related mitochondrial division was required for PTEN-mediated mitochondrial dysfunction and cell death. Finally, we found that PTEN modulated Drp1-related mitochondrial division via the Akt pathway; inactivation of Akt induced cell death, and mitochondrial damage, similar to the results obtained via PTEN overexpression. Conclusions: Taken together, our results clarify that the anticancer mechanism of PTEN in glioblastoma is dependent on the activation of Drp1-related mitochondrial division via Akt pathway modulation. This finding might provide new insight into the tumor-suppressive role played by PTEN in glioblastoma.