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首页> 外文期刊>The Journal of Nutritional Biochemistry >Flavokawain B inhibits growth of human squamous carcinoma cells: involvement of apoptosis and cell cycle dysregulation in vitro and in vivo.
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Flavokawain B inhibits growth of human squamous carcinoma cells: involvement of apoptosis and cell cycle dysregulation in vitro and in vivo.

机译：黄酮类固醇B抑制人鳞状细胞癌细胞的生长：在体外和体内都参与凋亡和细胞周期失调。

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摘要

Flavokawain B is a natural chalcone isolated from the rhizomes of Alpinia pricei Hayata. In the present study, we have investigated the antiproliferative and apoptotic effect of flavokawain B (5-20 mug/ml; 17.6-70.4 muM) against human squamous carcinoma (KB) cells. Exposure of KB cells with flavokawain B resulted in apoptosis, evidenced by loss of cell viability, profound morphological changes, genomic DNA fragmentation and sub-G1 phase accumulation. Apoptosis induced by flavokawain B results in activation of caspase-9, -3 and -8, cleavage of poly ADP ribose polymerase (PARP) and Bid in KB cells. Flavokawain B also down-regulate Bcl-2 with concomitant increase in Bax level, which resulted in release of cytochrome c. Taken together, the induction of apoptosis by flavokawain B involved in both death receptor and mitochondrial pathway. We also observed that flavokawain B caused the G2/M phase arrest that was mediated through reductions in the levels of cyclin A, cyclin B1, Cdc2 and Cdc25C and increases in p21/WAF1, Wee1 and p53 levels. Moreover, flavokawain B significantly inhibits matrix metalloproteinase-9 and urokinase plasminogen activator expression, whereas tissue inhibitor of matrix metalloproteinase-1 and plasminogen activator inhibitor-1 were increased, which are playing critical role in tumor metastasis. In addition, flavokawain B treatment significantly inhibited in vivo growth of human KB cell-derived tumor xenografts in nude mice, which is evidenced by augmentation of apoptotic DNA fragmentation, as detected by in situ terminal deoxynucleotidyl transferase-meditated dUTP nick end-labeling staining. The induction of cell cycle arrest and apoptosis by flavokawain B may provide a pivotal mechanism for its cancer chemopreventive action.
机译：Flavokawain B是从 Alpinia pricei Hayata的根茎中分离出来的天然查尔酮。在本研究中，我们研究了黄酮类固醇B（5-20​​杯/毫升; 17.6-70.4μM）对人鳞癌（KB）细胞的抗增殖和凋亡作用。黄酮类固醇B暴露于KB细胞会导致细胞凋亡，这可由细胞活力丧失，深刻的形态变化，基因组DNA片段化和亚G1期积累证明。黄酮类固醇B诱导的细胞凋亡导致caspase-9，-3和-8的激活，多ADP核糖聚合酶（PARP）的切割和KB细胞中的Bid的切割。 Flavokawain B还下调Bcl-2，同时Bax水平升高，导致细胞色素c释放。两者合计，黄素蛋白B诱导的凋亡参与死亡受体和线粒体途径。我们还观察到黄酮类固醇B引起G2 / M期停滞，这是通过降低细胞周期蛋白A，细胞周期蛋白B1，Cdc2和Cdc25C的水平以及增加p21 / WAF1，Wee1和p53的水平介导的。此外，黄酮类固醇B显着抑制基质金属蛋白酶9和尿激酶纤溶酶原激活物的表达，而基质金属蛋白酶-1和纤溶酶原激活物抑制物1的组织抑制剂增加，这在肿瘤转移中起关键作用。此外，黄酮类固醇B处理可显着抑制裸鼠体内人KB细胞源性肿瘤异种移植的体内生长，这可通过凋亡DNA片段化的增强来证明，如通过原位末端脱氧核苷酸转移酶修饰的dUTP缺口末端标记染色所检测到的。黄酮类固醇B诱导细胞周期停滞和凋亡可能为其癌症化学预防作用提供关键机制。

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