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芹菜素及其与伏立诺他的联合使用通过调节表观遗传和凋亡调节因子以及相关的微小RNA，诱导三阴性乳腺癌细胞发生凋亡介导的细胞死亡。

Apigenin and its combination with Vorinostat induces apoptotic-mediated cell death in TNBC by modulating the epigenetic and apoptotic regulators and related miRNAs.

作者信息

Nimal Snehal, Kumbhar Navanath, Rathore Shriya, Naik Nitin, Paymal Sneha, Gacche Rajesh N

机构信息

Department of Biotechnology, Savitribai Phule Pune University (SPPU), Pune, 411007, Maharashtra (MS), India.

Medical Information Management, Department of Biochemistry, Shivaji University, Kolhapur, 416004, Maharashtra (MS), India.

出版信息

Sci Rep. 2024 Apr 25;14(1):9540. doi: 10.1038/s41598-024-60395-x.

DOI:10.1038/s41598-024-60395-x
PMID:38664447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11045774/
Abstract

Triple-negative breast cancer (TNBC) is a metastatic disease and a formidable treatment challenge as it does not respond to existing therapies. Epigenetic regulators play a crucial role in the progression and metastasis by modulating the expression of anti-apoptotic, pro-apoptotic markers and related miRNAs in TNBC cells. We have investigated the anti-TNBC potential of dietary flavonoid 'Apigenin' and its combination with Vorinostat on MDA-MB-231 cells. At Apigenin generated ROS, inhibited cell migration, arrested the cell cycle at subG0/G1 phases, and induced apoptotic-mediated cell death. Apigenin reduced the expression of the class-I HDACs at the transcriptomic and proteomic levels. In the immunoblotting study, Apigenin has upregulated pro-apoptotic markers and downregulated anti-apoptotic proteins. Apigenin inhibited the enzymatic activity of HDAC/DNMT and increased HAT activity. Apigenin has manifested its effect on miRNA expression by upregulating the tumor-suppressor miR-200b and downregulation oncomiR-21. Combination study reduced the growth of TNBC cells synergistically by modulating the expression of epigenetic and apoptotic regulators. Molecular docking and MD simulations explored the mechanism of catalytic inhibition of HDAC1 and HDAC3 and supported the in-vitro studies. The overall studies demonstrated an anti-TNBC potential of Apigenin and may help to design an effective strategy to treat metastatic phenotype of TNBC.

摘要

三阴性乳腺癌（TNBC）是一种转移性疾病，由于其对现有治疗方法无反应，因此是一个严峻的治疗挑战。表观遗传调节因子通过调节TNBC细胞中抗凋亡、促凋亡标志物及相关微小RNA（miRNA）的表达，在肿瘤进展和转移中发挥关键作用。我们研究了膳食类黄酮“芹菜素”及其与伏立诺他联合对MDA-MB-231细胞的抗TNBC潜力。芹菜素可产生活性氧（ROS），抑制细胞迁移，使细胞周期停滞在亚G0/G1期，并诱导凋亡介导的细胞死亡。芹菜素在转录组和蛋白质组水平降低了I类组蛋白去乙酰化酶（HDAC）的表达。在免疫印迹研究中，芹菜素上调了促凋亡标志物，下调了抗凋亡蛋白。芹菜素抑制HDAC/DNA甲基转移酶（DNMT）的酶活性并增加组蛋白乙酰转移酶（HAT）活性。芹菜素通过上调肿瘤抑制性miR-200b和下调致癌性miR-21，对miRNA表达产生影响。联合研究通过调节表观遗传和凋亡调节因子的表达，协同降低了TNBC细胞的生长。分子对接和分子动力学模拟探索了HDAC1和HDAC3催化抑制的机制，并支持了体外研究。总体研究证明了芹菜素具有抗TNBC的潜力，可能有助于设计一种有效的策略来治疗TNBC的转移表型。

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