Breast carcinoma, one of the most lethal variants of carcinogenesis, significantly diagnosed type of cancer amongst the female population. Sinigrin, also known as glucosinolate, is found in the seeds of Brassica nigra and shown to enhance various cancer cells potentially. Nevertheless, the mechanistic explanation of SGN-mediated breast cancer growth and augmentation is still to be investigated. Hence, we contended in this study that SGN impedes PI3K/AKT/mTOR phosphorylation-mediated cell cycle arrest in MCF-7 cells. SGN (20 M) was implemented to treat MCF-7 cells for 24 and 48 hours of incubation. A significant increase in cytotoxicity, reactive oxygen species (ROS) generation, cell cycle arrest, mitochondrion membrane alteration, lipid peroxidation, and antioxidant depletion was found in MCF-7 cells. The PI3K/AKT/mTOR events are crucial pathways that participate in survival, proliferation, and cell cycle regulation. Inhibition of PI3K/AKT/mTOR expression thought to be novel approach for alleviating breast cancer growth. We noticed that SGN inhibits PI3K, AKT, and mTOR phosphorylation, resulting in the downregulation of proliferative and cell cycle regulatory proteins, such as cyclin-D1, PCNA, CDK4, and CDK6. SGN also causes apoptosis in MCF-7 cells by increasing nuclear fragmentation and by inducing pro-apoptotic gene expression. As a result, SGN inhibits breast cancer growth by impeding PI3K/AKT/mTOR phosphorylation-mediated cell cycle arrest in MCF-7 cells.

中文翻译：

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Sinigrin 通过抑制 PI3K/AKT/mTOR 磷酸化介导的细胞周期阻滞来阻止乳腺癌细胞的生长

乳腺癌是最致命的致癌变异之一，在女性人群中显着诊断出癌症类型。黑芥子苷，也称为硫代葡萄糖苷，存在于黑芥子的种子中，并显示出潜在地增强各种癌细胞的作用。然而，SGN 介导的乳腺癌生长和增大的机制解释仍有待研究。因此，我们在本研究中主张 SGN 阻碍 MCF-7 细胞中 PI3K/AKT/mTOR 磷酸化介导的细胞周期停滞。SGN (20 M) 用于处理 MCF-7 细胞 24 和 48 小时的孵育。在 MCF-7 细胞中发现细胞毒性、活性氧 (ROS) 生成、细胞周期停滞、线粒体膜改变、脂质过氧化和抗氧化剂消耗显着增加。PI3K/AKT/mTOR 事件是参与生存、增殖和细胞周期调节的关键途径。抑制 PI3K/AKT/mTOR 表达被认为是缓解乳腺癌生长的新方法。我们注意到 SGN 抑制 PI3K、AKT 和 mTOR 磷酸化，导致增殖和细胞周期调节蛋白的下调，例如 cyclin-D1、PCNA、CDK4 和 CDK6。SGN 还通过增加核碎片和诱导促凋亡基因表达导致 MCF-7 细胞凋亡。因此，SGN 通过阻止 PI3K/AKT/mTOR 磷酸化介导的 MCF-7 细胞中的细胞周期停滞来抑制乳腺癌的生长。我们注意到 SGN 抑制 PI3K、AKT 和 mTOR 磷酸化，导致增殖和细胞周期调节蛋白的下调，例如 cyclin-D1、PCNA、CDK4 和 CDK6。SGN 还通过增加核碎片和诱导促凋亡基因表达导致 MCF-7 细胞凋亡。因此，SGN 通过阻止 PI3K/AKT/mTOR 磷酸化介导的 MCF-7 细胞中的细胞周期停滞来抑制乳腺癌的生长。我们注意到 SGN 抑制 PI3K、AKT 和 mTOR 磷酸化，导致增殖和细胞周期调节蛋白的下调，例如 cyclin-D1、PCNA、CDK4 和 CDK6。SGN 还通过增加核碎片和诱导促凋亡基因表达导致 MCF-7 细胞凋亡。因此，SGN 通过阻止 PI3K/AKT/mTOR 磷酸化介导的 MCF-7 细胞中的细胞周期停滞来抑制乳腺癌的生长。