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藻类硫酸化卡拉胶通过凋亡调控基因抑制MDA-MB-231细胞的增殖。

Algal sulfated carrageenan inhibits proliferation of MDA-MB-231 cells via apoptosis regulatory genes.

作者信息

Murad Hossam, Ghannam Ahmed, Al-Ktaifani Mahmoud, Abbas Assef, Hawat Mohammad

机构信息

Department of Molecular Biology and Biotechnology, Atomic Energy Commission of Syria, P.O. Box 6091, Damascus, Syria.

Department of Chemistry, Atomic Energy Commission of Syria, P.O. Box 6091, Damascus, Syria.

出版信息

Mol Med Rep. 2015 Mar;11(3):2153-8. doi: 10.3892/mmr.2014.2915. Epub 2014 Nov 10.

DOI:10.3892/mmr.2014.2915
PMID:25384757
Abstract

Marine algae are prolific sources of sulfated polysaccharides, which may explain the low incidence of certain cancers in countries that traditionally consume marine food. Breast cancer is one of the most common types of non‑skin cancer in females. In this study, extracted sulfated carrageenan (ESC), predominantly consisting of ι‑carrageenan extracted from the red alga Laurencia papillosa, was characterized using Fourier transform infrared spectrometry. The biological effects of the identified extract were investigated and its potential cytotoxic activity was tested against the MDA‑MB‑231 cancer cell line. The biological biometer of the inhibitory concentration of the polysaccharide‑treated MDA‑MB‑231 cells was determined as 50 µM. Treatment with 50 µM ESC inhibited cell proliferation and promptly induced cell death through nuclear condensation and DNA fragmentation. Characterization of polysaccharide‑treated MDA‑MB‑231 cell death revealed that induction of apoptosis occurred via the activation of the extrinsic apoptotic caspase‑8 gene. The apoptotic signaling pathway was regulated through caspase‑3, caspase‑9, p53, Bax and Bcl‑2 genes. These findings suggest that ESC may serve as a potential therapeutic agent to target breast cancer via prompting apoptosis.

摘要

海藻是硫酸化多糖的丰富来源,这或许可以解释在传统上食用海产品的国家中某些癌症发病率较低的现象。乳腺癌是女性中最常见的非皮肤癌类型之一。在本研究中,使用傅里叶变换红外光谱法对主要由从红藻乳头凹顶藻中提取的ι-卡拉胶组成的提取硫酸化卡拉胶(ESC)进行了表征。研究了所鉴定提取物的生物学效应,并测试了其对MDA-MB-231癌细胞系的潜在细胞毒性活性。多糖处理的MDA-MB-231细胞的抑制浓度的生物学测定值为50μM。用50μM ESC处理可抑制细胞增殖,并通过核浓缩和DNA片段化迅速诱导细胞死亡。对多糖处理的MDA-MB-231细胞死亡的表征显示,凋亡的诱导是通过激活外源性凋亡半胱天冬酶-8基因发生的。凋亡信号通路通过半胱天冬酶-3、半胱天冬酶-9、p53、Bax和Bcl-2基因进行调节。这些发现表明,ESC可能作为一种潜在的治疗剂,通过促进凋亡来靶向乳腺癌。

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