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撤回文章：阿柔比星通过SIRT1/PI3K/AKT信号通路调节胶质瘤细胞生长和DNA损伤。

Retracted Article: Aclarubicin regulates glioma cell growth and DNA damage through the SIRT1/PI3K/AKT signaling pathway.

作者信息

Huo Jun-Feng, Chen Xiao-Bing

机构信息

Second Ward, Department of Neurosurgery, Huaihe Hospital of Henan University No. 8 Baobei Road Kaifeng 475000 Henan province China

出版信息

RSC Adv. 2019 Sep 12;9(49):28775-28782. doi: 10.1039/c9ra05572j. eCollection 2019 Sep 9.

DOI:10.1039/c9ra05572j
PMID:35529648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9071234/
Abstract

Aclarubicin (ACR), an anthracycline anti-tumor agent, is known to play important roles in cancer. Evidence has suggested that ACR has therapeutic effects on rats intracranially implanted with C6 glioma cells. However, the function and mechanism of ACR in glioma cells remain elusive. In this study, we examined the effects of ACR on glioma cell growth, apoptosis, and DNA damage. Our results showed that treatment with different concentrations of ACR (1, 2, and 5 μM) markedly impeded glioma cell survival, significantly decreased cell proliferation, and increased cell apoptosis and caspase-3 activity. Furthermore, ACR treatment promoted DNA damage through phosphorylation of ATM and CHK1 in U87 and U251 cells. Treatment with ACR also increased sirtuin 1 (SIRT1) expression and inhibited phosphatidylinositol 3'-kinase (PI3K)/AKT pathway activation. Interestingly, we found that AKT overexpression reversed the effects of ACR on glioma cell survival, proliferation, apoptosis, and DNA damage. Thus, our data suggest that ACR induces apoptosis and DNA damage in U87 and U251 cells through the SIRT1/PI3K/AKT signaling pathway.

摘要

阿柔比星（ACR）是一种蒽环类抗肿瘤药物，已知其在癌症中发挥重要作用。有证据表明，ACR对颅内植入C6胶质瘤细胞的大鼠具有治疗作用。然而，ACR在胶质瘤细胞中的功能和机制仍不清楚。在本研究中，我们检测了ACR对胶质瘤细胞生长、凋亡和DNA损伤的影响。我们的结果表明，用不同浓度的ACR（1、2和5 μM）处理可显著阻碍胶质瘤细胞存活，显著降低细胞增殖，并增加细胞凋亡和半胱天冬酶-3活性。此外，ACR处理通过U87和U251细胞中ATM和CHK1的磷酸化促进DNA损伤。ACR处理还增加了沉默调节蛋白1（SIRT1）的表达并抑制磷脂酰肌醇3'-激酶（PI3K）/AKT途径的激活。有趣的是，我们发现AKT过表达可逆转ACR对胶质瘤细胞存活、增殖、凋亡和DNA损伤的影响。因此，我们的数据表明，ACR通过SIRT1/PI3K/AKT信号通路诱导U87和U251细胞凋亡和DNA损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/f635dc8bb5ba/c9ra05572j-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/f6443a5b4117/c9ra05572j-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/3022a7d68802/c9ra05572j-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/d2e784c383be/c9ra05572j-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/4c5837a8e9ce/c9ra05572j-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/be3cc0f51f20/c9ra05572j-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/f635dc8bb5ba/c9ra05572j-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/f6443a5b4117/c9ra05572j-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/3022a7d68802/c9ra05572j-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/d2e784c383be/c9ra05572j-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/4c5837a8e9ce/c9ra05572j-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/be3cc0f51f20/c9ra05572j-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/726c/9071234/f635dc8bb5ba/c9ra05572j-f6.jpg

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本文引用的文献

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ESMO Open. 2019 Jun 17;4(Suppl 2):e000520. doi: 10.1136/esmoopen-2019-000520. eCollection 2019.
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Mol Med Rep. 2018 Feb;17(2):2757-2763. doi: 10.3892/mmr.2017.8132. Epub 2017 Nov 22.
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