Zexia Wang1, Fei Liu2, Wenli Liao3, Liangzhu Yu4, Zhenwu Hu5, Mincai Li6, Hongli Xia7. 1. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China; Department of Pharmacy, Henan Shengde Hospital, Xinyang, 464000, PR China. Electronic address: 454544454@qq.com. 2. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China; School of Pharmacy, Hubei University of Science and Technology, Xianning, 437100, PR China. Electronic address: 2440032910@qq.com. 3. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China. Electronic address: roxana822@163.com. 4. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China. Electronic address: yuliangyu73@163.com. 5. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China. Electronic address: huzhenwu@hotmail.com. 6. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China; School of Pharmacy, Hubei University of Science and Technology, Xianning, 437100, PR China. Electronic address: mincaili@163.com. 7. School of Basic Medical Sciences, Hubei University of Science and Technology, Xianning, 437100, PR China; The Central Hospital of Xianning, Hubei University of Science and Technology, Xianning, 437100, PR China. Electronic address: mobei_hu@126.com.
Abstract
BACKGROUND: Glioblastoma (GB) is the most common neoplasm in the brain. Curcumin, as a known polyphenolic compound extracted from turmeric, is a chemotherapy used in some cancer treatments in China. However, the effect of curcumin on the survivability of GB cells remains to be elucidated. METHODS: We performed a CCK8 assay to detect the viability of GB cells following treatments with curcumin and examined the migration and invasion the ability of these cells using the wound-healing and transwell invasion assays. The cell proliferation and apoptotic proteins were detected by Western blot analyses. We utilized a glioblastoma-xenograft mouse model to assess cell proliferation following curcumin treatment. RESULTS: We found that curcumin inhibited the proliferation, migration, and invasion of U251 and U87 GB cells. We detected that curcumin decreased p-AKT and p-mTOR protein expression, and promoted the apoptosis of U251 and U87 GB cells. Further, we found that curcumin promoted the PTEN and p53 expression, as the tumor suppressor genes. In addition, we administered curcumin to nude mice and found that curcumin decreased the tumor volume, caused necrosis of tumor tissue, and significantly enhanced the PTEN and p53 expression in vivo. CONCLUSIONS: These results indicated that curcumin inhibited proliferation by decreasing the p-AKT/p-mTOR pathway and promoted apoptosis by increasing the PTEN and p53 expression. Our study provided the molecular mechanisms by which curcumin inhibited glioblastoma and its targeted interventions.
BACKGROUND:Glioblastoma (GB) is the most common neoplasm in the brain. Curcumin, as a known polyphenolic compound extracted from turmeric, is a chemotherapy used in some cancer treatments in China. However, the effect of curcumin on the survivability of GB cells remains to be elucidated. METHODS: We performed a CCK8 assay to detect the viability of GB cells following treatments with curcumin and examined the migration and invasion the ability of these cells using the wound-healing and transwell invasion assays. The cell proliferation and apoptotic proteins were detected by Western blot analyses. We utilized a glioblastoma-xenograft mouse model to assess cell proliferation following curcumin treatment. RESULTS: We found that curcumin inhibited the proliferation, migration, and invasion of U251 and U87 GB cells. We detected that curcumin decreased p-AKT and p-mTOR protein expression, and promoted the apoptosis of U251 and U87 GB cells. Further, we found that curcumin promoted the PTEN and p53 expression, as the tumor suppressor genes. In addition, we administered curcumin to nude mice and found that curcumin decreased the tumor volume, caused necrosis of tumor tissue, and significantly enhanced the PTEN and p53 expression in vivo. CONCLUSIONS: These results indicated that curcumin inhibited proliferation by decreasing the p-AKT/p-mTOR pathway and promoted apoptosis by increasing the PTEN and p53 expression. Our study provided the molecular mechanisms by which curcumin inhibited glioblastoma and its targeted interventions.
Authors: Sarah C Kammerud; Brandon J Metge; Amr R Elhamamsy; Shannon E Weeks; Heba A Alsheikh; Alexa L Mattheyses; Lalita A Shevde; Rajeev S Samant Journal: Lab Invest Date: 2021-07-15 Impact factor: 5.662