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海洋蒽醌 SZ-685C 通过抑制 Akt 信号通路克服乳腺癌细胞对阿霉素的耐药性。

A marine anthraquinone SZ-685C overrides adriamycin-resistance in breast cancer cells through suppressing Akt signaling.

机构信息

Key Laboratory of Tropical Disease Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.

Guangdong Province Key Laboratory of Functional Molecules in Oceanic Microorganism (Sun Yat-sen University), Bureau of Education, Guangzhou 510080, China.

出版信息

Mar Drugs. 2012 Apr;10(4):694-711. doi: 10.3390/md10040694. Epub 2012 Mar 23.

DOI:10.3390/md10040694
PMID:22690138
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3366670/
Abstract

Breast cancer remains a major health problem worldwide. While chemotherapy represents an important therapeutic modality against breast cancer, limitations in the clinical use of chemotherapy remain formidable because of chemoresistance. The HER2/PI-3K/Akt pathway has been demonstrated to play a causal role in conferring a broad chemoresistance in breast cancer cells and thus justified to be a target for enhancing the effects of anti-breast cancer chemotherapies, such as adriamycin (ADR). Agents that can either enhance the effects of chemotherapeutics or overcome chemoresistance are urgently needed for the treatment of breast cancer. In this context, SZ-685C, an agent that has been previously shown, as such, to suppress Akt signaling, is expected to increase the efficacy of chemotherapy. Our current study investigated whether SZ-685C can override chemoresistance through inhibiting Akt signaling in human breast cancer cells. ADR-resistant cells derived from human breast cancer cell lines MCF-7, MCF-7/ADR and MCF-7/Akt, were used as models to test the effects of SZ-685C. We found that SZ-685C suppressed the Akt pathway and induced apoptosis in MCF-7/ADR and MCF-7/Akt cells that are resistant to ADR treatment, leading to antitumor effects both in vitro and in vivo. Our data suggest that use of SZ-685C might represent a potentially promising approach to the treatment of ADR-resistant breast cancer.

摘要

乳腺癌仍然是全球范围内的一个主要健康问题。虽然化疗是治疗乳腺癌的一种重要方法，但由于化疗耐药性的存在，其在临床上的应用仍存在很大的局限性。HER2/PI-3K/Akt 通路已被证明在赋予乳腺癌细胞广泛的化疗耐药性方面起着因果作用，因此被认为是增强抗乳腺癌化疗效果的靶点，如阿霉素（ADR）。能够增强化疗效果或克服化疗耐药性的药物对于乳腺癌的治疗是迫切需要的。在这种情况下，SZ-685C 是一种先前被证明能够抑制 Akt 信号的药物，预计它可以提高化疗的疗效。我们目前的研究调查了 SZ-685C 是否可以通过抑制 Akt 信号来克服人类乳腺癌细胞中的化疗耐药性。从人乳腺癌细胞系 MCF-7、MCF-7/ADR 和 MCF-7/Akt 中获得的 ADR 耐药细胞被用作模型来测试 SZ-685C 的作用。我们发现 SZ-685C 抑制了 Akt 通路，并诱导对 ADR 治疗耐药的 MCF-7/ADR 和 MCF-7/Akt 细胞凋亡，从而在体外和体内均产生了抗肿瘤作用。我们的数据表明，使用 SZ-685C 可能代表一种有前途的治疗 ADR 耐药性乳腺癌的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/8bf4f6b0c7b5/marinedrugs-10-00694-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/3a7b82cef45b/marinedrugs-10-00694-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/83727e0c5c8c/marinedrugs-10-00694-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/0812b40d1c8e/marinedrugs-10-00694-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/16a0c99e7d59/marinedrugs-10-00694-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/8bf4f6b0c7b5/marinedrugs-10-00694-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/3a7b82cef45b/marinedrugs-10-00694-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/83727e0c5c8c/marinedrugs-10-00694-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/0812b40d1c8e/marinedrugs-10-00694-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/16a0c99e7d59/marinedrugs-10-00694-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fade/3366670/8bf4f6b0c7b5/marinedrugs-10-00694-g005.jpg

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本文引用的文献

1
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Acta Biochim Biophys Sin (Shanghai). 2011 Aug;43(8):647-53. doi: 10.1093/abbs/gmr050. Epub 2011 Jun 28.
2
Cancer statistics, 2010.癌症统计数据，2010 年。
CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300. doi: 10.3322/caac.20073. Epub 2010 Jul 7.
3
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Naunyn Schmiedebergs Arch Pharmacol. 2025 Apr;398(4):3321-3343. doi: 10.1007/s00210-024-03579-6. Epub 2024 Nov 16.
4
SZ-685C inhibits the growth of non-functioning pituitary adenoma by down-regulating miR-340-3p and inducing autophagy.SZ-685C通过下调miR-340-3p并诱导自噬来抑制无功能垂体腺瘤的生长。
Heliyon. 2024 Aug 30;10(17):e37230. doi: 10.1016/j.heliyon.2024.e37230. eCollection 2024 Sep 15.
5
Chemical diversity, medicinal potentialities, biosynthesis, and pharmacokinetics of anthraquinones and their congeners derived from marine fungi: a comprehensive update.海洋真菌来源蒽醌及其类似物的化学多样性、药用潜力、生物合成和药代动力学：全面更新
RSC Adv. 2022 Sep 1;12(38):24887-24921. doi: 10.1039/d2ra03610j. eCollection 2022 Aug 30.
6
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8
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Br J Pharmacol. 2010 Feb 1;159(3):689-97. doi: 10.1111/j.1476-5381.2009.00577.x. Epub 2010 Jan 28.
4
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Nat Rev Drug Discov. 2009 Jan;8(1):69-85. doi: 10.1038/nrd2487. Epub 2008 Dec 19.
5
PI3K pathway alterations in cancer: variations on a theme.癌症中PI3K信号通路的改变：同一主题的变体
Oncogene. 2008 Sep 18;27(41):5497-510. doi: 10.1038/onc.2008.245.
6
Anthracycline cardiotoxicity: from bench to bedside.蒽环类药物心脏毒性：从 bench 到 bedside。 注：bench 直译为“实验台”，bedside 直译为“床边”，这里意译为从基础研究到临床应用。
J Clin Oncol. 2008 Aug 1;26(22):3777-84. doi: 10.1200/JCO.2007.14.9401.
7
Cellular mechanisms of resistance to anthracyclines and taxanes in cancer: intrinsic and acquired.癌症中对蒽环类药物和紫杉烷类药物耐药的细胞机制：内在性和获得性。
Semin Oncol. 2008 Apr;35(2 Suppl 2):S1-S14; quiz S39. doi: 10.1053/j.seminoncol.2008.02.010.
8
Chemically targeting the PI3K family.化学靶向PI3K家族。
Biochem Soc Trans. 2007 Apr;35(Pt 2):245-9. doi: 10.1042/BST0350245.
9
HER2 and responsiveness of breast cancer to adjuvant chemotherapy.人表皮生长因子受体2（HER2）与乳腺癌对辅助化疗的反应性
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10
Targeting multidrug resistance in cancer.针对癌症中的多药耐药性
Nat Rev Drug Discov. 2006 Mar;5(3):219-34. doi: 10.1038/nrd1984.