Radiation Biology Department, Radiation Research Division, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt.
Lab of molecular Biology, Zoology Department, Faculty of Science, Al Azhar University, Cairo, Egypt.
Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231180849. doi: 10.1177/09603271231180849.
Treatment strategies encompass synchronization of more than one therapy with specific dependence on zeroing side effects of natural products that might represent a niche in the continuous struggle against cancer. Thus, this study aimed at assessing the role of WS (Ashwagandha) in forcing MCF7 or MDA-MB 231 irradiated breast cancer cells to outweigh the route of programmed cell death. We check to what extent SIRT1-BCL2/Bax signaling pathway was interrelated to form apoptotic cancer cells. MDA or MCF7 cells are categorized into four groups: gp1, Control (C): MDA-MB-231 or MCF7 cells not treated with WS or exposed to γ-rays, gp2 (WS): cells challenged with WS for MDA-MB-231 or MCF7 cells respectively, gp3: irradiated (R) MDA-MB-231 or MCF7 cells exposed to γ-rays (4 Gy; one shot) and gp4 WS and irradiated (WS + R): cells challenged with WS as in gp2 and exposed to gamma rays as in gp3. The results revealed that, WS established IC equivalent to 4897.8 μg/ml in MDA-MB-231 cells or equivalent to 3801.9 μg/ml in MCF7 cells. The flowcytometric analysis (Annexin V and cell cycle) showed that WS induces apoptosis at pre-G phase and induces cell arrest at G2/M and preG1 phases for MDA-MB-231 and at the preG1 for MCF7 cells. Furthermore, the WS + R group of cells (MDA-MB-231 and MCF7) showed significant increases in the expression of SIRT1, and BCL2 and a decrease in BAX compared with WS or R group. It could be concluded that WS has an anti-proliferative action on MDA-MB-231 and MCF7 cells because of its capability to enhance apoptosis.
治疗策略包括同步多种治疗方法，并特别依赖于消除天然产物的副作用，这可能是对抗癌症的一个新途径。因此，本研究旨在评估 WS（印度人参）在迫使 MCF7 或 MDA-MB-231 照射乳腺癌细胞选择程序性细胞死亡途径方面的作用。我们检查 SIRT1-BCL2/Bax 信号通路在多大程度上相互关联，以形成凋亡癌细胞。MDA 或 MCF7 细胞分为四组：gp1，对照（C）：未用 WS 处理或未暴露于γ射线的 MDA-MB-231 或 MCF7 细胞，gp2（WS）：分别用 WS 处理 MDA-MB-231 或 MCF7 细胞的细胞，gp3：照射（R）MDA-MB-231 或 MCF7 细胞暴露于γ射线（4Gy；单次）和 gp4 WS 和照射（WS+R）：用 WS 处理如 gp2 所示并用γ射线处理如 gp3 所示的细胞。结果表明，WS 在 MDA-MB-231 细胞中建立的 IC 等效于 4897.8μg/ml，在 MCF7 细胞中建立的 IC 等效于 3801.9μg/ml。流式细胞术分析（Annexin V 和细胞周期）表明，WS 在 MDA-MB-231 细胞中诱导 G0/G1 期前的细胞凋亡，并诱导 G2/M 和 G0/G1 期前的细胞停滞，而在 MCF7 细胞中诱导 G0/G1 期前的细胞停滞。此外，WS+R 组（MDA-MB-231 和 MCF7）细胞的 SIRT1、BCL2 表达显著增加，BAX 表达显著降低与 WS 或 R 组相比。可以得出结论，WS 对 MDA-MB-231 和 MCF7 细胞具有抗增殖作用，因为它能够增强细胞凋亡。
