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诱导乳腺癌细胞死亡:紫杉醇对通过凋亡实现增殖的影响。

Inducing breast cancer cell death: The impact of taxodone on proliferation through apoptosis.

作者信息

Bakhsh Tahani, Alyami Nouf M

机构信息

Department of Biology, College of Science, University of Jeddah, Jeddah, 21589, Saudi Arabia.

Department of Zoology, College of Science, King Saud University, PO Box -2455, Riyadh, 11451, Saudi Arabia.

出版信息

Heliyon. 2024 Jul 4;10(13):e34044. doi: 10.1016/j.heliyon.2024.e34044. eCollection 2024 Jul 15.

Abstract

Breast cancer is the most prevalent form of cancer in women and a major contributor to cancer-related fatalities worldwide. Several factors play a role in the development of breast cancer, encompassing age, hormone levels, etc. Taxodone has shown significant anti-tumor properties in both laboratory experiments and living organisms. However, its impact on the human MCF-7 breast cancer cell line has not been researched. This investigation explores the chemo-preventive potential of taxodone in the MCF-7 breast cancer cells. The anticancer potential of taxodone against MCF-7 cells was determined by MTT assay. Further, the induction of apoptosis in MCF-7 breast cancer cells was confirmed via ELISA, which indicated the increased incidences of chromatin condensation and ssDNA breakage in the MCF-7 apoptotic cells upon 24 h of taxodone treatment. The intracellular reactive oxygen species (ROS) level was evaluated using HDCFDA fluorescent dye to elucidate the mechanism of action triggered upon taxodone treatment. The increasing intercellular ROS level sequentially activated the caspase-mediated apoptosis pathway. Consequently, the outcomes revealed that taxodone decreased the cell viability of MCF-7 dose-dependently. Taxodone triggers apoptosis in MCF-7 cells by increasing intracellular ROS levels and activating the caspase cascade through the mitochondrial apoptosis-induced channel, an early marker of apoptosis onset. Our results indicate that taxodone exhibits anti-proliferative and apoptotic properties against human MCF-7 breast cancer cells, suggesting it to be a natural anticancer agent.

摘要

乳腺癌是女性中最常见的癌症形式,也是全球癌症相关死亡的主要原因之一。乳腺癌的发生涉及多个因素,包括年龄、激素水平等。在实验室实验和生物体中,紫杉酮均显示出显著的抗肿瘤特性。然而,其对人MCF-7乳腺癌细胞系的影响尚未得到研究。本研究探讨了紫杉酮在MCF-7乳腺癌细胞中的化学预防潜力。通过MTT法测定了紫杉酮对MCF-7细胞的抗癌潜力。此外,通过ELISA证实了MCF-7乳腺癌细胞中凋亡的诱导,这表明在紫杉酮处理24小时后,MCF-7凋亡细胞中染色质浓缩和单链DNA断裂的发生率增加。使用HDCFDA荧光染料评估细胞内活性氧(ROS)水平,以阐明紫杉酮处理后触发的作用机制。细胞内ROS水平的升高依次激活了半胱天冬酶介导的凋亡途径。因此,结果显示紫杉酮剂量依赖性地降低了MCF-7的细胞活力。紫杉酮通过增加细胞内ROS水平并通过线粒体凋亡诱导通道激活半胱天冬酶级联反应,从而触发MCF-7细胞凋亡,这是凋亡开始的早期标志物。我们的结果表明,紫杉酮对人MCF-7乳腺癌细胞具有抗增殖和凋亡特性,表明它是一种天然抗癌剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec6/11269907/67bc52d61af5/gr1.jpg

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