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黄芩苷诱导的自噬涉及体外 SMMC-7721 细胞中 CD147 的下调。

Autophagy induced by baicalin involves downregulation of CD147 in SMMC-7721 cells in vitro.

机构信息

School of Medicine, Xi'an Jiaotong University, Xi'an, PR China.

出版信息

Oncol Rep. 2012 Apr;27(4):1128-34. doi: 10.3892/or.2011.1599. Epub 2011 Dec 20.

Abstract

Baicalin has been demonstrated to exert anticancer effects mainly through induction of tumor cell apoptosis and cell cycle arrest. However, the precise mechanisms underlying its anticancer role remain to be elucidated. In the present study, we investigated whether autophagy was involved in the anticancer activity of baicalin in the human hepatocellular carcinoma (HCC) cell line SMMC-7721 and the possible molecular mechanisms. Our data showed that the viability of SMMC-7721 cells was significantly inhibited by baicalin in a dose- and time-dependent manner. Alongside apoptosis, autophagy was also induced by baicalin dose- and time-dependently with the involvement of the autophagy-associated protein Βeclin 1. Moreover, we demonstrated that cell death induced by baicalin was significantly inhibited by the apoptosis inhibitor z-DEVD-fmk or the autophagy inhibitor 3-MA, respectively. In addition, we found that CD147, a key molecule related both to apoptosis and autophagy, was markedly downregulated at the protein level in SMMC-7721 cells treated with baicalin. Collectively, this is the first study to suggest that baicalin induces autophagic cell death in SMMC-7721 cells, which involves the downregulation of CD147. Our study reveals a new mechanism for the anticancer effects of baicalin and puts forward a potential crucial role of CD147 in baicalin-induced cancer cell death.

摘要

黄芩素主要通过诱导肿瘤细胞凋亡和细胞周期阻滞发挥抗癌作用。然而,其抗癌作用的确切机制仍有待阐明。在本研究中,我们研究了自噬是否参与黄芩素在人肝癌(HCC)细胞系 SMMC-7721 中的抗癌活性及其可能的分子机制。我们的数据表明,黄芩素在剂量和时间依赖性方式下显著抑制 SMMC-7721 细胞的活力。除了凋亡,黄芩素还剂量和时间依赖性地诱导自噬,涉及自噬相关蛋白 Βeclin 1。此外,我们证明凋亡抑制剂 z-DEVD-fmk 或自噬抑制剂 3-MA 分别显著抑制黄芩素诱导的细胞死亡。此外,我们发现黄芩素处理的 SMMC-7721 细胞中,与凋亡和自噬均相关的关键分子 CD147 的蛋白水平显著下调。总之,这是第一项表明黄芩素诱导 SMMC-7721 细胞发生自噬性细胞死亡的研究,涉及 CD147 的下调。我们的研究揭示了黄芩素抗癌作用的新机制,并提出了 CD147 在黄芩素诱导的癌细胞死亡中的潜在关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccdc/3583557/4bbacd0353bd/OR-27-04-1128-g0.jpg

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