Growth inhibitory efficacy of the nutritional herb Psoralea corylifolia in a model of triple‑negative breast cancer

N. Telang, H. Nair, G. Wong
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引用次数: 4

Abstract

. Triple‑negative breast cancer (TNBC) lacks the expression of estrogen receptor‑ α (ER‑ α ), progesterone receptor (PR) and amplified human epidermal growth factor receptor‑2 (HER‑2). Current treatments involve chemo‑ therapy and molecular targeted therapy. These options lead to dose‑limiting systemic toxicity and acquired tumor resis‑ tance. Moreover, no drug is yet available for the secondary prevention of TNBC. Such limitations underscore a need to investigate non‑toxic testable alternatives for the secondary prevention/treatment of TNBC. The Chinese nutritional herb, Psoralea corylifolia (PC), has been shown to be effective against the MCF‑7 cell line, a cellular model for ER‑ α ‑positive breast cancer. The present study aimed to investigate the growth inhibitory effects of PC against TNBC using the MDA‑MB‑231 cell line. Anchorage‑independent colony forma‑ tion, cell cycle progression, cellular apoptosis, RB signaling and caspase‑3/7 activity assays were performed to determine the quantitative parameters for the efficacy of PC. Treatment with PC induced a 3.5‑fold increase in the G 1 : S + G 2 /M ratio, an 11‑fold increase in the apoptotic cell number and a 149‑fold increase in caspase‑3/7 activity. PC treatment also decreased cyclin D1, CDK4/6 and p‑RB expression levels. On the whole, the data of the present study identify mechanistic leads for PC as a naturally occurring testable alternative, and validate a mechanistic approach to prioritize efficacious nontoxic herbal extracts as nutritional supplements for the secondary preven‑ tion/therapy of TNBC.
营养草药补骨脂对三阴性乳腺癌模型的生长抑制作用
. 三阴性乳腺癌(TNBC)缺乏雌激素受体α (ER - α)、孕激素受体(PR)和扩增的人表皮生长因子受体2 (HER - 2)的表达。目前的治疗方法包括化疗和分子靶向治疗。这些选择导致剂量限制性全身毒性和获得性肿瘤阻抗。此外,目前还没有药物可用于TNBC的二级预防。这些局限性强调了研究三阴癌二级预防/治疗的无毒可测试替代品的必要性。中国营养草药补骨脂(Psoralea corylifolia, PC)已被证明对MCF - 7细胞系有效,MCF - 7细胞系是ER - α阳性乳腺癌的细胞模型。本研究旨在利用MDA - MB - 231细胞系研究PC对TNBC的生长抑制作用。通过锚定不依赖的集落形成、细胞周期进展、细胞凋亡、RB信号和caspase‑3/7活性测定来确定PC疗效的定量参数。PC处理诱导g1: S + g2 /M比值增加3.5倍,凋亡细胞数量增加11倍,caspase - 3/7活性增加149倍。PC处理也降低了cyclin D1、CDK4/6和p - RB的表达水平。总的来说,本研究的数据确定了PC作为一种自然存在的可测试替代品的机制线索,并验证了优先考虑有效无毒草药提取物作为TNBC二级预防/治疗的营养补充剂的机制方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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