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.
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.
Arch Biochem Biophys. 2020 Aug 15;689:108412. doi: 10.1016/j.abb.2020.108412. Epub 2020 May 21.
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.
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.
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.
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.
胶质母细胞瘤（GB）是最常见的脑肿瘤。姜黄素是一种从姜黄中提取的已知多酚化合物，在中国一些癌症治疗中被用作化疗药物。然而，姜黄素对 GB 细胞存活率的影响仍需阐明。
我们通过 CCK8 法检测姜黄素处理后 GB 细胞的活力，并通过划痕愈合和 Transwell 侵袭实验检测这些细胞的迁移和侵袭能力。通过 Western blot 分析检测细胞增殖和凋亡蛋白。我们利用胶质母细胞瘤异种移植小鼠模型来评估姜黄素处理后细胞的增殖情况。
我们发现姜黄素抑制 U251 和 U87GB 细胞的增殖、迁移和侵袭。我们检测到姜黄素降低了 p-AKT 和 p-mTOR 蛋白的表达，并促进了 U251 和 U87GB 细胞的凋亡。此外，我们发现姜黄素促进了肿瘤抑制基因 PTEN 和 p53 的表达。此外，我们给裸鼠施用姜黄素，发现姜黄素降低了肿瘤体积，导致肿瘤组织坏死，并显著增强了体内的 PTEN 和 p53 表达。
这些结果表明，姜黄素通过降低 p-AKT/p-mTOR 通路来抑制增殖，并通过增加 PTEN 和 p53 表达来促进凋亡。我们的研究提供了姜黄素抑制胶质母细胞瘤及其靶向干预的分子机制。
