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天然化合物角鲨烯通过活性氧依赖途径诱导 A549 肺癌细胞中的 DNA 损伤和凋亡及体外评价。

Natural compound chaetocin induced DNA damage and apoptosis through reactive oxygen species-dependent pathways in A549 lung cancer cells and in vitro evaluations.

机构信息

TCM Teaching and Research Office, Leshan Vocational and Technical College, Leshan, China.

Department of Oncology, Leshan Hospital of Traditional Chinese Medicine, Leshan, China.

出版信息

IET Nanobiotechnol. 2023 Jul;17(5):465-475. doi: 10.1049/nbt2.12144. Epub 2023 Jul 7.

DOI:10.1049/nbt2.12144
PMID:37417682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10374551/
Abstract

There is an urgent need for potential pharmaceutics for lung cancer treatment due to the increased number of lung cancer deaths and the resistance of cancer cells to present therapeutics. The present work aims to discover the anticancer potential of the natural compound chaetocin as a therapeutic for lung cancer treatment. Results showed the significance of chaetocin-induced cell growth inhibition by the expression of G /M phase arrest and reactive oxygen species (ROS) dependent apoptosis in A549 lung cancer cells. Results concluded that chaetocin could produce ROS and nuclear damage against A549 lung cancer cells. Interestingly, chaetocin exhibits a significant level of CD47 that down-regulates the expression of CD47 at mRNA levels. PBMC biocompatibility study revealed that chaetocin is non-toxic to normal cells. Overall, experimental results suggested that chaetocin induces A549 cell apoptosis, by causing ROS and nuclear damage activation pathways. In the future, chaetocin might be an effective bio-safe anticancer agent for lung cancer treatments.

摘要

由于肺癌死亡人数的增加以及癌细胞对现有疗法的耐药性，迫切需要寻找治疗肺癌的潜在药物。本研究旨在探索天然化合物头抱菌素作为肺癌治疗药物的抗癌潜力。结果表明，头抱菌素通过 A549 肺癌细胞中 G/M 期阻滞和活性氧（ROS）依赖性凋亡的表达，显著抑制细胞生长。结果表明，头抱菌素可以产生 ROS 和核损伤，对抗 A549 肺癌细胞。有趣的是，头抱菌素表现出显著水平的 CD47，下调 CD47 在 mRNA 水平的表达。PBMC 细胞相容性研究表明，头抱菌素对正常细胞没有毒性。总的来说，实验结果表明，头抱菌素通过诱导 ROS 和核损伤激活途径诱导 A549 细胞凋亡。在未来，头抱菌素可能成为一种有效的生物安全抗癌药物，用于治疗肺癌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ca98f03698de/NBT2-17-465-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ff14695b2676/NBT2-17-465-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/8d06689f3f80/NBT2-17-465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/a43c71c75d46/NBT2-17-465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/717011ddc9b5/NBT2-17-465-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/5dc2f2279a1e/NBT2-17-465-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/66370a13bfa2/NBT2-17-465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ccd4934fbdf3/NBT2-17-465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/0756e42d1b7e/NBT2-17-465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ca98f03698de/NBT2-17-465-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ff14695b2676/NBT2-17-465-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/8d06689f3f80/NBT2-17-465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/a43c71c75d46/NBT2-17-465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/717011ddc9b5/NBT2-17-465-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/5dc2f2279a1e/NBT2-17-465-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/66370a13bfa2/NBT2-17-465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ccd4934fbdf3/NBT2-17-465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/0756e42d1b7e/NBT2-17-465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4869/10374551/ca98f03698de/NBT2-17-465-g006.jpg

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