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芳樟醇和1,8-桉叶素对非小细胞肺癌A549细胞的抗癌机制

Anti-cancer mechanisms of linalool and 1,8-cineole in non-small cell lung cancer A549 cells.

作者信息

Rodenak-Kladniew Boris, Castro María Agustina, Crespo Rosana, Galle Marianela, García de Bravo Margarita

机构信息

Instituto de Investigaciones Bioquímicas de La Plata (INIBIOLP), CONICET-UNLP, CCT-La Plata La Plata, Argentina.

Cátedra de Biología, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina.

出版信息

Heliyon. 2020 Dec 15;6(12):e05639. doi: 10.1016/j.heliyon.2020.e05639. eCollection 2020 Dec.

DOI:10.1016/j.heliyon.2020.e05639
PMID:33367122
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7749389/
Abstract

Linalool and 1,8-cineole are plant-derived isoprenoids with anticancer activities in lung cancer cells, nevertheless, the cellular and molecular mechanisms of action remain poorly understood. The purpose of this study was to determine the anticancer mechanisms of action of linalool and 1,8-cineole in lung adenocarcinoma A549 cells. Linalool (0-2.0 mM) and 1,8-cineole (0-8.0 mM) inhibited cell proliferation by inducing G0/G1 and/or G2/M cell cycle arrest without affecting cell viability of normal lung WI-38 cells. None of the two monoterpenes were able to induce apoptosis, as observed by the lack of caspase-3 and caspase-9 activation, PARP cleavage, and DNA fragmentation. Linalool, but not 1,8-cineole, increased reactive oxygen species production and mitochondrial membrane potential depolarization. Reactive oxygen species were involved in cell growth inhibition and mitochondrial depolarization induced by linalool since the antioxidant N-acetyl-L-cysteine prevented both effects. Besides, linalool (2.0 mM) and 1,8-cineole (8.0 mM) inhibited A549 cell migration. The combination of each monoterpene with simvastatin increased the G0/G1 cell cycle arrest and sensitized cells to apoptosis compared with simvastatin alone. Our results showed that both monoterpenes might be promising anticancer agents with antiproliferative, anti-metastatic, and sensitizer properties for lung cancer therapy.

摘要

芳樟醇和1,8-桉叶素是植物来源的类异戊二烯，对肺癌细胞具有抗癌活性，然而，其细胞和分子作用机制仍知之甚少。本研究的目的是确定芳樟醇和1,8-桉叶素在肺腺癌A549细胞中的抗癌作用机制。芳樟醇（0 - 2.0 mM）和1,8-桉叶素（0 - 8.0 mM）通过诱导G0/G1和/或G2/M期细胞周期阻滞来抑制细胞增殖，而不影响正常肺WI-38细胞的活力。这两种单萜均未诱导细胞凋亡，这可通过缺乏caspase-3和caspase-9激活、PARP裂解及DNA片段化来观察到。芳樟醇而非1,8-桉叶素可增加活性氧生成及线粒体膜电位去极化。活性氧参与了芳樟醇诱导的细胞生长抑制和线粒体去极化，因为抗氧化剂N-乙酰-L-半胱氨酸可阻止这两种效应。此外，芳樟醇（2.0 mM）和1,8-桉叶素（8.0 mM）可抑制A549细胞迁移。与单独使用辛伐他汀相比，每种单萜与辛伐他汀联合使用可增加G0/G1期细胞周期阻滞并使细胞对凋亡敏感。我们的结果表明，这两种单萜可能是有前景的抗癌药物，具有抗增殖、抗转移及增敏特性，可用于肺癌治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/66e2546619e0/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/a200416a432e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/8e551dcc159e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/b6b8472f3cb8/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/c81630752b4c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/d829678527a4/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/8b9c91724ee4/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/f76dfe7c73bf/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/66e2546619e0/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/a200416a432e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/8e551dcc159e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/b6b8472f3cb8/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/c81630752b4c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/d829678527a4/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/8b9c91724ee4/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/f76dfe7c73bf/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227e/7749389/66e2546619e0/figs1.jpg

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