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吖啶酮衍生物通过 ERK 通路抑制癌细胞增殖。

Acridone Derivatives from Inhibited Cancer Cell Proliferation through ERK Pathway.

机构信息

Faculty of Pharmaceutical Sciences, Ubon Ratchathani University, Ubon Ratchathani 34190, Thailand.

Faculty of Pharmaceutical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand.

出版信息

Molecules. 2022 Jun 16;27(12):3865. doi: 10.3390/molecules27123865.

DOI:10.3390/molecules27123865
PMID:35744993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9228231/
Abstract

The present study aimed to investigate the effect of acridone alkaloids on cancer cell lines and elucidate the underlying molecular mechanisms. The ten acridone alkaloids from were screened for cytotoxicity against LNCaP cell lines by a WST-8 assay. Then, the most potential acridone, buxifoliadine E, was evaluated on four types of cancer cells, namely prostate cancer (LNCaP), neuroblastoma (SH SY5Y), hepatoblastoma (HepG2), and colorectal cancer (HT29). The results showed that buxifoliadine E was able to significantly inhibit the proliferation of all four types of cancer cells, having the most potent cytotoxicity against the HepG2 cell line. Western blotting analysis was performed to assess the expression of signaling proteins in the cancer cells. In HepG2 cells, buxifoliadine E induced changes in the levels of Bid as well as cleaved caspase-3 and Bax through MAPKs, including Erk and p38. Moreover, the binding interaction between buxifoliadine E and Erk was investigated by using the Autodock 4.2.6 and Discovery Studio programs. The result showed that buxifoliadine E bound at the ATP-binding site, located at the interface between the N- and C-terminal lobes of Erk2. The results of this study indicate that buxifoliadine E suppressed cancer cell proliferation by inhibiting the Erk pathway.

摘要

本研究旨在探讨吖啶酮生物碱对癌细胞系的影响，并阐明其潜在的分子机制。采用 WST-8 法筛选 中的 10 种吖啶酮生物碱对 LNCaP 细胞系的细胞毒性。然后，对四种类型的癌细胞（前列腺癌（LNCaP）、神经母细胞瘤（SH SY5Y）、肝癌（HepG2）和结直肠癌（HT29））评估最有潜力的吖啶酮，即 buxifoliadine E。结果表明，buxifoliadine E 能够显著抑制四种类型的癌细胞增殖，对 HepG2 细胞系的细胞毒性最强。通过 Western blotting 分析评估了癌症细胞中信号蛋白的表达。在 HepG2 细胞中，buxifoliadine E 通过 MAPKs（包括 Erk 和 p38）诱导 Bid 以及 cleaved caspase-3 和 Bax 的水平发生变化。此外，还使用 Autodock 4.2.6 和 Discovery Studio 程序研究了 buxifoliadine E 与 Erk 之间的结合相互作用。结果表明，buxifoliadine E 结合在 Erk2 的 N-和 C-末端结构域之间的 ATP 结合位点上。本研究结果表明，buxifoliadine E 通过抑制 Erk 通路抑制癌细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/5aa5b3181d3b/molecules-27-03865-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/00a63448d4bb/molecules-27-03865-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/7b0841bb214e/molecules-27-03865-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/7217f38e2845/molecules-27-03865-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/363bf45dcc3a/molecules-27-03865-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/41cd3039dc55/molecules-27-03865-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/df8df1939247/molecules-27-03865-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/be344d5ed7d8/molecules-27-03865-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/87940c44e296/molecules-27-03865-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/7a7398c31432/molecules-27-03865-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/6b328775a324/molecules-27-03865-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/db10fb38f27d/molecules-27-03865-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/2406bbcbb50b/molecules-27-03865-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/5aa5b3181d3b/molecules-27-03865-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/00a63448d4bb/molecules-27-03865-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/7b0841bb214e/molecules-27-03865-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/7217f38e2845/molecules-27-03865-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/363bf45dcc3a/molecules-27-03865-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/41cd3039dc55/molecules-27-03865-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/df8df1939247/molecules-27-03865-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/be344d5ed7d8/molecules-27-03865-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/87940c44e296/molecules-27-03865-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/7a7398c31432/molecules-27-03865-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/6b328775a324/molecules-27-03865-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/db10fb38f27d/molecules-27-03865-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/2406bbcbb50b/molecules-27-03865-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d69b/9228231/5aa5b3181d3b/molecules-27-03865-g013.jpg

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