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环菠萝酮联合阿霉素通过 ROS 生成和 NRF2/ARE 信号通路诱导 MCF-7 和 MCF-7/ADR 癌细胞凋亡。

Cyperotundone combined with adriamycin induces apoptosis in MCF-7 and MCF-7/ADR cancer cells by ROS generation and NRF2/ARE signaling pathway.

机构信息

First Clinical College, Shandong University of Traditional Chinese Medicine, Jinan, 250014, Shandong, People's Republic of China.

Breast Cancer CenterShandong Cancer Hospital and Institute, Shandong Academy of Medical Sciences, Shandong First Medical University, Jinan, 250117, Shandong, People's Republic of China.

出版信息

Sci Rep. 2023 Jan 25;13(1):1384. doi: 10.1038/s41598-022-26767-x.

DOI:10.1038/s41598-022-26767-x
PMID:36697441
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9877033/
Abstract

Breast cancer has become the most prevalent cancer, globally. Adriamycin is a first-line chemotherapeutic agent, however, cancer cells acquire resistance to it, which is one of the most common causes of treatment failure. ROS and NRF2 are essential oxidative stress factors that play a key role in the oxidative stress process and are associated with cancer. Our goal is to create novel therapeutic drugs or chemical sensitizers that will improve chemotherapy sensitivity. The optimal concentration and duration for MCF-7 and MCF-7/ADR cells in ADR and CYT were determined using the CCK-8 assay. We found that ADR + CYT inhibited the activity of MCF-7 and MCF-7/ADR cells in breast cancer, as well as causing apoptosis in MCF-7 and MCF-7/ADR cells and blocking the cell cycle in the G0/G1 phase. ADR + CYT induces apoptosis in MCF-7 and MCF-7/ADR cells through ROS generation and the P62/NRF2/HO-1 signaling pathway. In breast cancer-bearing nude mice, ADR + CYT effectively suppressed tumor development in vivo. Overall, our findings showed that CYT in combination with ADR has potent anti-breast cancer cell activity both in vivo and in vitro, suggesting CYT as the main drug used to improve chemosensitivity.

摘要

乳腺癌已成为全球最普遍的癌症。阿霉素是一种一线化疗药物，然而，癌细胞对其产生了耐药性，这是治疗失败的最常见原因之一。ROS 和 NRF2 是至关重要的氧化应激因素，在氧化应激过程中发挥着关键作用，并与癌症有关。我们的目标是创造新的治疗药物或化学增敏剂，以提高化疗敏感性。使用 CCK-8 测定法确定了 MCF-7 和 MCF-7/ADR 细胞在 ADR 和 CYT 中的最佳浓度和时间。我们发现 ADR+CYT 抑制了乳腺癌 MCF-7 和 MCF-7/ADR 细胞的活性，导致 MCF-7 和 MCF-7/ADR 细胞凋亡，并阻止细胞周期进入 G0/G1 期。ADR+CYT 通过 ROS 生成和 P62/NRF2/HO-1 信号通路诱导 MCF-7 和 MCF-7/ADR 细胞凋亡。在荷瘤裸鼠中，ADR+CYT 有效地抑制了体内肿瘤的发展。总的来说，我们的研究结果表明，CYT 与 ADR 联合具有强大的抗乳腺癌细胞活性，无论是在体内还是体外，提示 CYT 是提高化疗敏感性的主要药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/aeebf5aa2e3d/41598_2022_26767_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/2e836e4726a6/41598_2022_26767_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/aeebf5aa2e3d/41598_2022_26767_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/2e836e4726a6/41598_2022_26767_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/83e2f3e905a1/41598_2022_26767_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/2ee106bc52ba/41598_2022_26767_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5de6/9877033/3fc2fd2c5b48/41598_2022_26767_Fig6_HTML.jpg
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