银格丁通过抑制NRF2-HO-1轴活动来增强乳腺癌放射治疗的敏感性
Qiong Duan1, Zhenting Cui1, Mingxiao Wang2
1The Affiliated Lianyungang Municipal Oriental Hospital of Xuzhou Medical University, Lianyungang 222042, Jiangsu, China.
Toxicology and applied pharmacology
|December 9, 2024
概括
基丁通过诱导放射性抵抗细胞中的铁亡来增强乳腺癌放射疗法. 这种天然化合物显示出克服治疗耐药性和改善患者结果的潜力.
科学领域:
- 在瘤学瘤学.
- 药理学 药理学是指药理学的学科.
- 生物化学 生化学
背景情况:
- 乳腺癌 (BC) 在全球范围内对女性构成重大健康风险.
- 放射治疗 (RT) 是BC的关键治疗方法,但放射电阻限制了其有效性.
- 基丁 (GK) 是一种天然化合物,具有与铁亡相关的抗瘤特性.
研究的目的:
- 研究基丁 (GK) 克服乳腺癌 (BC) 放射电阻的机制.
- 评估GK在增强BC细胞对放射治疗 (RT) 的敏感性方面的潜力.
主要方法:
- 使用了体外和体外实验模型.
- 评估了GK对BC细胞生长,细胞亡和铁亡的影响.
- 分析了NRF2,HO-1,NQO1,ROS,铁离子,GSH和GPX4表达的变化.
主要成果:
- 银格丁抑制了BC细胞的生长,并增加了细胞亡.
- 在抗辐射BC细胞中,GK通过减少NRF2,HO-1和NQO1.1来促进铁亡.
- GK增加了活性氧物种 (ROS) 和铁离子,减少了谷氨 (GSH),并降低了GPX4表达,同时损害了线粒体.
结论:
- 银素有效地促进放射抵抗性乳腺癌细胞中的铁亡.
- GK在提高乳腺癌放射治疗敏感度方面显示出显著的潜力.
- 这项研究提供了Ginkgetin作为放射敏感剂的证据,用于未来的临床应用.
更多相关视频
相关概念视频
Targeted Cancer Therapies
7.5K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
There are several types of targeted therapies against...
7.5K
Mitogens and the Cell Cycle
6.4K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.4K
Inhibition of Cdk Activity
4.7K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.7K
mTOR Signaling and Cancer Progression
3.7K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
3.7K


