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α-茄碱对 MCF-7 人腺癌细胞的细胞毒性作用取决于其在孵育介质中与胆固醇的相互作用，并不涉及细胞凋亡诱导。

The cytotoxic effect of α-tomatine in MCF-7 human adenocarcinoma breast cancer cells depends on its interaction with cholesterol in incubation media and does not involve apoptosis induction.

机构信息

Department of Medical Biochemistry, Charles University in Prague, Faculty of Medicine in Hradec Kralove, Hradec Kralove, Czech Republic.

出版信息

Oncol Rep. 2013 Dec;30(6):2593-602. doi: 10.3892/or.2013.2778. Epub 2013 Oct 2.

DOI:10.3892/or.2013.2778
PMID:24100733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3839989/
Abstract

In recent years, α-tomatine has been studied for its anticancer activity. In the present study, we focused on the cytotoxic effect of α-tomatine in the MCF-7 human breast adenocarcinoma cell line, its mechanism of action, biotransformation and stability in the culture medium. We observed an inhibition of cell proliferation and viability at concentrations of 6 and 9 µM but then a recovery of cells occurred. The recovery was not caused by the biotransformation of α-tomatine in MCF-7 cells, but by a substantial decrease in the concentration of α-tomatine in the culture medium due to its binding with cholesterol. Regarding the mechanism of action of α-tomatine, we observed no DNA damage, no changes in the levels of the proteins p53 and p21(WAF1/Cip1), and no apoptosis (neither activated caspase-8 and -9, nor sub-G1 peak, or morphological signs). We found a loss of ATP in α-tomatine-treated cells. These results support the conclusion that α-tomatine does not induce apoptosis in the MCF-7 cell line.

摘要

近年来，α-茄碱的抗癌活性受到了研究关注。在本研究中，我们专注于 α-茄碱对 MCF-7 人乳腺癌腺癌细胞系的细胞毒性作用、作用机制、生物转化和在培养基中的稳定性。我们观察到在 6 和 9 μM 浓度下抑制细胞增殖和活力，但随后细胞恢复。这种恢复不是由 MCF-7 细胞中 α-茄碱的生物转化引起的，而是由于 α-茄碱与胆固醇结合，导致培养基中 α-茄碱浓度大幅下降。关于 α-茄碱的作用机制，我们没有观察到 DNA 损伤，p53 和 p21(WAF1/Cip1) 蛋白水平没有变化，也没有细胞凋亡（既没有激活的 caspase-8 和 caspase-9，也没有亚 G1 峰或形态学迹象）。我们发现 α-茄碱处理的细胞中 ATP 丢失。这些结果支持 α-茄碱不会诱导 MCF-7 细胞系细胞凋亡的结论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/ac544c98d9b7/OR-30-06-2593-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/3552946ddd0c/OR-30-06-2593-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/fd0f875e4c42/OR-30-06-2593-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/852a229d46cb/OR-30-06-2593-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/979c7cffea4e/OR-30-06-2593-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/ac544c98d9b7/OR-30-06-2593-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/3552946ddd0c/OR-30-06-2593-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/fd0f875e4c42/OR-30-06-2593-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/852a229d46cb/OR-30-06-2593-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/979c7cffea4e/OR-30-06-2593-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f9d2/3839989/ac544c98d9b7/OR-30-06-2593-g04.jpg

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