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表棓儿茶素 E 降低三阴性乳腺癌细胞系 MDA-MB-231 的侵袭性。

Ampelopsin E Reduces the Invasiveness of the Triple Negative Breast Cancer Cell Line, MDA-MB-231.

机构信息

Department of Biomedical Sciences, Faculty of Medicine and Health Science, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia.

Laboratory of Molecular Biomedicine, Institute of Bioscience, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia.

出版信息

Molecules. 2019 Jul 18;24(14):2619. doi: 10.3390/molecules24142619.

DOI:10.3390/molecules24142619
PMID:31323836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6680398/
Abstract

Breast cancer is the most common and the second leading cause of cancer-related deaths in women. It has two distinctive hallmarks: rapid abnormal growth and the ability to invade and metastasize. During metastasis, cancer cells are thought to form actin-rich protrusions, called invadopodia, which degrade the extracellular matrix. Current breast cancer treatments, particularly chemotherapy, comes with adverse effects like immunosuppression, resistance development and secondary tumour formation. Hence, naturally-occurring molecules claimed to be less toxic are being studied as new drug candidates. Ampelopsin E, a natural oligostilbene extracted from species, has exhibited various pharmacological properties, including anticancer and anti-inflammatory activities. However, there is yet no scientific evidence of the effects of ampelopsin E towards metastasis. Scratch assay, transwell migration and invasion assays, invadopodia and gelatin degradation assays, and ELISA were used to determine the effects of ampelopsin E towards the invasiveness of MDA-MB-231 cells. Strikingly in this study, ampelopsin E was able to halt migration, transmigration and invasion in MDA-MB-231 cells by reducing formation of invadopodia and its degradation capability through significant reduction ( < 0.05) in expression levels of PDGF, MMP2, MMP9 and MMP14. In conclusion, ampelopsin E reduced the invasiveness of MDA-MB-231 cells and was proven to be a potential alternative in treating TNBC.

摘要

乳腺癌是女性最常见和第二大癌症相关死亡原因。它有两个显著的特征：快速异常生长和侵袭转移的能力。在转移过程中，癌细胞被认为形成富含肌动蛋白的突起，称为侵袭伪足，它们降解细胞外基质。目前的乳腺癌治疗方法，特别是化疗，伴随着免疫抑制、耐药性发展和继发性肿瘤形成等不良反应。因此，正在研究天然存在的、据称毒性较小的分子作为新的药物候选物。从 种中提取的天然低聚二苯乙烯 Ampelopsin E 表现出多种药理特性，包括抗癌和抗炎活性。然而，目前还没有 Ampelopsin E 对转移影响的科学证据。划痕实验、Transwell 迁移和侵袭实验、侵袭伪足和明胶降解实验以及 ELISA 用于确定 Ampelopsin E 对 MDA-MB-231 细胞侵袭性的影响。在这项研究中，令人惊讶的是，Ampelopsin E 通过显著降低（<0.05） PDGF、MMP2、MMP9 和 MMP14 的表达水平，减少侵袭伪足的形成及其降解能力，从而能够阻止 MDA-MB-231 细胞的迁移、转染和侵袭。总之，Ampelopsin E 降低了 MDA-MB-231 细胞的侵袭性，被证明是治疗三阴性乳腺癌的一种潜在替代方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/9fb02b7e28cf/molecules-24-02619-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/297771c210c2/molecules-24-02619-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/41ad3c94ddf4/molecules-24-02619-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/2d74fe0180b8/molecules-24-02619-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/bbeb8d1b12ab/molecules-24-02619-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/b89dadc6f773/molecules-24-02619-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/56bcc0115e97/molecules-24-02619-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/1f54e6fa3d32/molecules-24-02619-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/dbe253de96e2/molecules-24-02619-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/9fb02b7e28cf/molecules-24-02619-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/297771c210c2/molecules-24-02619-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/41ad3c94ddf4/molecules-24-02619-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/2d74fe0180b8/molecules-24-02619-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/bbeb8d1b12ab/molecules-24-02619-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/b89dadc6f773/molecules-24-02619-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/56bcc0115e97/molecules-24-02619-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/1f54e6fa3d32/molecules-24-02619-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/dbe253de96e2/molecules-24-02619-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8add/6680398/9fb02b7e28cf/molecules-24-02619-g009.jpg

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