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L. 对三阴性乳腺癌细胞的治疗作用。

The treatment role of L. to triple-negative breast cancer cells.

机构信息

Department of Oncology, Shandong Cancer Hospital affiliated to Shandong University, Shandong Academy of Medical Sciences, Jinan, Shandong 250017, China.

Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, China.

出版信息

Biosci Rep. 2019 Jun 7;39(6). doi: 10.1042/BSR20190502. Print 2019 Jun 28.

DOI:10.1042/BSR20190502
PMID:31123166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6554218/
Abstract

L. is widely used in Traditional Chinese Medicine and studies have reported its anticancer effect, but its chemical composition and therapy mechanism remains unknown. This research aims to analyze the chemical components of the ethanol extract of L. (EECR), detect its treatment effects on human Triple-negative breast cancer (TNBC) cells, and elucidate possible therapy mechanisms. The chemical components of EECR were detected by the Waters UPLC combined with Bruker Q-TOF mass spectrometer (UPLC-Q-TOF-MS). The phytochemical compounds were identified by comparing the mass fragmentations of each metabolite with databases such as METLIN, HMDB, and NCBI. A total of 21 compounds were identified in EECR. MDA-MB-231 and MDA-MB-468 cells were treated with various concentrations of EECR. Cell proliferation was examined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell apoptosis and cell cycle were detected by flow cytometry. Apoptosis- and autophagy-related protein expression was detected by Western blot. EECR inhibits the proliferation of TNBC cells (MDA-MB-231 and MDA-MB-468) in a dose-dependent manner, which may be related to the arrest of cell cycle in G/G phase. It induces apoptosis by promoting the expression of BAX and inhibiting the expression of BCL-2. In addition, autophagy inhibitor 3-Methyladenine (3-MA) inhibited TNBC cells pro-survival autophagy and increased the sensitivity of EECR. The present results demonstrated that EECR has potential effects on inhibits the proliferation and induction apoptosis in TNBC.

摘要

党参在中医药中被广泛应用,研究报道其具有抗癌作用,但党参的化学成分和治疗机制尚不清楚。本研究旨在分析党参乙醇提取物(EECR)的化学成分,检测其对人三阴性乳腺癌(TNBC)细胞的治疗作用,并阐明可能的治疗机制。采用沃特世 UPLC 结合布鲁克 Q-TOF 质谱仪(UPLC-Q-TOF-MS)检测 EECR 的化学成分。通过比较每个代谢物的质谱碎片与 METLIN、HMDB 和 NCBI 等数据库,鉴定出植物化学成分。在 EECR 中共鉴定出 21 种化合物。用不同浓度的 EECR 处理 MDA-MB-231 和 MDA-MB-468 细胞。用细胞计数试剂盒-8(CCK-8)和集落形成实验检测细胞增殖。用流式细胞术检测细胞凋亡和细胞周期。用 Western blot 检测凋亡和自噬相关蛋白的表达。EECR 呈剂量依赖性抑制 TNBC 细胞(MDA-MB-231 和 MDA-MB-468)的增殖,这可能与细胞周期在 G1/G0 期的阻滞有关。它通过促进 BAX 的表达和抑制 BCL-2 的表达来诱导细胞凋亡。此外,自噬抑制剂 3-甲基腺嘌呤(3-MA)抑制了 TNBC 细胞的生存自噬,并增加了 EECR 的敏感性。本研究结果表明,EECR 对抑制 TNBC 的增殖和诱导凋亡具有潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/d65add956ac4/bsr-39-bsr20190502-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/c8cd06b3140d/bsr-39-bsr20190502-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/0107393a93d6/bsr-39-bsr20190502-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/816c458a409c/bsr-39-bsr20190502-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/f63d1da155f8/bsr-39-bsr20190502-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/b0dcd90149c4/bsr-39-bsr20190502-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/d65add956ac4/bsr-39-bsr20190502-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/c8cd06b3140d/bsr-39-bsr20190502-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/0107393a93d6/bsr-39-bsr20190502-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/816c458a409c/bsr-39-bsr20190502-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/f63d1da155f8/bsr-39-bsr20190502-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/b0dcd90149c4/bsr-39-bsr20190502-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e8b/6554218/d65add956ac4/bsr-39-bsr20190502-g6.jpg

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