Bisdemethoxycurcumin Induces Cell Apoptosis and Inhibits Human Brain Glioblastoma GBM 8401/Luc2 Cell Xenograft Tumor in Subcutaneous Nude Mice In Vivo.
Bisdemethoxycurcumin Induces Cell Apoptosis and Inhibits Human Brain Glioblastoma GBM 8401/Luc2 Cell Xenograft Tumor in Subcutaneous Nude Mice In Vivo.
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DOI：
10.3390/ijms23010538
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发表时间：
2022-01-04
影响因子：
5.6
通讯作者：
Wu RS
中科院分区：
文献类型：
--
作者：
Hsia TC;Peng SF;Chueh FS;Lu KW;Yang JL;Huang AC;Hsu FT;Wu RS
双去甲氧基姜黄素（BDMC）具有生物活性，包括体外抗癌作用；然而，其对人类胶质母细胞瘤（GBM）细胞的抗癌作用尚未被研究。本研究旨在体外和体内研究BDMC对人GBM 8401/luc2细胞的抑瘤作用及其分子机制。体外研究表明，BDMC可显著降低GBM 8401/luc2细胞的细胞活力，诱导细胞凋亡。此外，BDMC通过抑制Bcl-2（抗凋亡蛋白）、增加Bax（促凋亡蛋白）和细胞色素c在体外诱导GBM 8401/luc2细胞凋亡。将12只BALB/c裸鼠皮下移植人胶质母细胞瘤GBM 8401/luc2癌细胞，每3 d分别给予BDMC 30和60 mg/kg处理。GBM 8401/luc2细胞异种移植实验表明，两种剂量的BDMC均能显著抑制肿瘤的生长，这是基于肿瘤大小和重量的减少。BDMC对大鼠体重和肝脏H&E组织病理学分析均无影响，说明BDMC未引起全身毒性。同时，与对照组相比，BDMC上调了肿瘤组织中BAX和cleaved caspase-3的表达，下调了Bcl-2和XIAP的蛋白表达。本研究表明，BDMC通过诱导细胞凋亡和抑制肿瘤细胞增殖，对人胶质母细胞瘤GBM 8401/luc2细胞异种移植模型具有较强的抗肿瘤活性，具有进一步开发抗GBM肿瘤药物的潜力。
Bisdemethoxycurcumin (BDMC) has biological activities, including anticancer effects in vitro; however, its anticancer effects in human glioblastoma (GBM) cells have not been examined yet. This study aimed to evaluate the tumor inhibitory effect and molecular mechanism of BDMC on human GBM 8401/luc2 cells in vitro and in vivo. In vitro studies have shown that BDMC significantly reduced cell viability and induced cell apoptosis in GBM 8401/luc2 cells. Furthermore, BDMC induced apoptosis via inhibited Bcl-2 (anti-apoptotic protein) and increased Bax (pro-apoptotic proteins) and cytochrome c release in GBM 8401/luc2 cells in vitro. Then, twelve BALB/c-nude mice were xenografted with human glioblastoma GBM 8401/luc2 cancer cells subcutaneously, and the xenograft nude mice were treated without and with BDMC (30 and 60 mg/kg of BDMC treatment) every 3 days. GBM 8401/luc2 cell xenografts experiment showed that the growth of the tumors was significantly suppressed by BDMC administration at both doses based on the reduction of tumor size and weights. BDMC did not change the body weight and the H&E histopathology analysis of liver samples, indicating that BDMC did not induce systemic toxicity. Meanwhile, treatment with BDMC up-regulated the expressions of BAX and cleaved caspase-3, while it down-regulated the protein expressions of Bcl-2 and XIAP in the tumor tissues compared with the control group. This study has demonstrated that BDMC presents potent anticancer activity on the human glioblastoma GBM 8401/luc2 cell xenograft model by inducing apoptosis and inhibiting tumor cell proliferation and shows the potential for further development to the anti-GBM cancer drug.
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