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探讨类黄酮木樨草素诱导 U-251 细胞死亡的机制:深入了解其对神经胶质瘤的抗癌特性。

Investigation of U-251 cell death triggered by flavonoid luteolin: towards a better understanding on its anticancer property against glioblastomas.

机构信息

Research Laboratory in Molecular Pharmacology of Bioactive Compounds, São Francisco University - Bragança Paulista, São Paulo, Brazil.

Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, São Paulo, Brazil.

出版信息

Nat Prod Res. 2021 Nov;35(22):4807-4813. doi: 10.1080/14786419.2020.1727470. Epub 2020 Feb 21.

DOI:10.1080/14786419.2020.1727470
PMID:32081041
Abstract

Recently, many studies have reported the anticancer properties of flavonoid luteolin against a variety of tumors, but there is still a lack in the description of its mechanism of action. In attempt to better contribute to the literature, we evaluated the antiproliferative activity of luteolin extracted by in a panel of tumor cell lines representative of six different tissues. Luteolin presented antiproliferative activity for all the assessed tumor cell lines, being glioblastoma the most sensitive one. This compound was able to inhibit U-251 cells migration and tumorigenesis. Besides, luteolin leads U-251 tumor cells to apoptosis death by depolarisation of the mitochondrial membrane, ERK proteins phosphorylation, cleavage of PARP and Caspase 9, further inducing DNA damage by H2AX phosphorylation, which had not yet been described for glioblastomas. Altogether, our results reaffirm luteolin as a potential therapeutic drug.

摘要

最近,许多研究报告了类黄酮木犀草素对多种肿瘤的抗癌特性,但对其作用机制的描述仍不够充分。为了更好地为文献做出贡献,我们评估了[方法]提取的木犀草素在一组代表六种不同组织的肿瘤细胞系中的增殖抑制活性。木犀草素对所有评估的肿瘤细胞系均表现出增殖抑制活性,其中神经胶质瘤最为敏感。该化合物能够抑制 U-251 细胞的迁移和致瘤性。此外,木犀草素通过线粒体膜去极化、ERK 蛋白磷酸化、PARP 和 Caspase 9 的切割,导致 U-251 肿瘤细胞凋亡死亡,进一步通过 H2AX 磷酸化诱导 DNA 损伤,这在神经胶质瘤中尚未被描述过。总之,我们的研究结果再次证实木犀草素是一种潜在的治疗药物。

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Investigation of U-251 cell death triggered by flavonoid luteolin: towards a better understanding on its anticancer property against glioblastomas.探讨类黄酮木樨草素诱导 U-251 细胞死亡的机制:深入了解其对神经胶质瘤的抗癌特性。
Nat Prod Res. 2021 Nov;35(22):4807-4813. doi: 10.1080/14786419.2020.1727470. Epub 2020 Feb 21.
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