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大麻二酚诱导人胃癌 SGC-7901 细胞的细胞周期停滞和细胞凋亡。

Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells.

机构信息

Yantai Key Laboratory of Pharmacology of Traditional Chinese Medicine in Tumor Metabolism, School of Integrated Traditional Chinese and Western Medicine, Binzhou Medical University, Yantai 264003, China.

School of Gerontology, Binzhou Medical University, Yantai 264003, China.

出版信息

Biomolecules. 2019 Jul 25;9(8):302. doi: 10.3390/biom9080302.

DOI:10.3390/biom9080302
PMID:31349651
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6723681/
Abstract

The main chemical component of cannabis, cannabidiol (CBD), has been shown to have antitumor properties. The present study examined the in vitro effects of CBD on human gastric cancer SGC-7901 cells. We found that CBD significantly inhibited the proliferation and colony formation of SGC-7901 cells. Further investigation showed that CBD significantly upregulated ataxia telangiectasia-mutated gene (ATM) and p53 protein expression and downregulated p21 protein expression in SGC-7901 cells, which subsequently inhibited the levels of CDK2 and cyclin E, thereby resulting in cell cycle arrest at the G0-G1 phase. In addition, CBD significantly increased Bax expression levels, decreased Bcl-2 expression levels and mitochondrial membrane potential, and then upregulated the levels of cleaved caspase-3 and cleaved caspase-9, thereby inducing apoptosis in SGC-7901 cells. Finally, we found that intracellular reactive oxygen species (ROS) increased after CBD treatment. These results indicated that CBD could induce G0-G1 phase cell cycle arrest and apoptosis by increasing ROS production, leading to the inhibition of SGC-7901 cell proliferation, thereby suggesting that CBD may have therapeutic effects on gastric cancer.

摘要

大麻的主要化学成分大麻二酚(CBD)已被证明具有抗肿瘤特性。本研究探讨了 CBD 对人胃癌 SGC-7901 细胞的体外作用。我们发现 CBD 能显著抑制 SGC-7901 细胞的增殖和集落形成。进一步的研究表明,CBD 能显著上调 SGC-7901 细胞中的共济失调毛细血管扩张突变基因(ATM)和 p53 蛋白的表达,下调 p21 蛋白的表达,从而抑制 CDK2 和细胞周期蛋白 E 的水平,导致细胞周期停滞在 G0-G1 期。此外,CBD 能显著增加 Bax 蛋白的表达水平,降低 Bcl-2 蛋白的表达水平和线粒体膜电位,然后上调 cleaved caspase-3 和 cleaved caspase-9 的水平,从而诱导 SGC-7901 细胞凋亡。最后,我们发现 CBD 处理后细胞内活性氧(ROS)增加。这些结果表明,CBD 通过增加 ROS 的产生,诱导 G0-G1 期细胞周期阻滞和细胞凋亡,从而抑制 SGC-7901 细胞的增殖,提示 CBD 可能对胃癌具有治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/38aba1e4c959/biomolecules-09-00302-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/e6df57a9ec76/biomolecules-09-00302-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/cab6280b8001/biomolecules-09-00302-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/5a7e7c05c4db/biomolecules-09-00302-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/abc2176ebdf1/biomolecules-09-00302-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/f5ef910d5e47/biomolecules-09-00302-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/6b8efef63f9a/biomolecules-09-00302-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/38aba1e4c959/biomolecules-09-00302-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/e6df57a9ec76/biomolecules-09-00302-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/cab6280b8001/biomolecules-09-00302-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/5a7e7c05c4db/biomolecules-09-00302-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/abc2176ebdf1/biomolecules-09-00302-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/f5ef910d5e47/biomolecules-09-00302-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/6b8efef63f9a/biomolecules-09-00302-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9863/6723681/38aba1e4c959/biomolecules-09-00302-g007.jpg

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