黄素通过抑制通过AKT/MMP14通路的侵袭来抑制膀癌
Kai Wang1, Wen Xiao2,3, Qi Zeng4
1Department of Pharmacy, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), 410006 Changsha, Hunan, China.
Discovery medicine
|January 26, 2024
概括
黄素通过抑制细胞入侵,显示出治疗膀癌的潜力. 这项研究揭示了黄素抑制了繁殖和迁移,同时通过AKT/MMP14通路促进了细胞亡.
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 生物化学
背景情况:
- 膀癌对健康构成重大威胁,需要新的治疗药物.
- 目前用于膀癌的治疗选择需要加强.
- 探索像黄素这样的天然化合物为药物开发提供了一个有前途的途径.
研究的目的:
- 为了研究黄素对膀癌的抑制作用.
- 阐明黄素在膀癌中作用的潜在分子机制.
- 确定黄素在膀癌治疗中的关键分子标.
主要方法:
- 网络药理学确定了膀癌中黄素的潜在点.
- 生物信息分析和免疫组织化学验证了矩阵金属蛋白酶-14 (MMP14) 作为一个关键目标.
- 在体外测试 (CCK-8,克隆形成,亡,Transwell) 评估了黄素对膀癌细胞的影响.
- 西部斑点分析检查了AKT/MMP14信号通路.
主要成果:
- 黄素的标包括STAT3,AKT,CCNA2,EGFR,EP300和MMP14. 这些黄素的标包括STAT3,AKT,CCNA2,EGFR,EP300和MMP14.
- 膀癌组织中MMP14表达升高,与预后不佳相关.
- 黄素显著抑制了膀癌细胞的扩散和迁移.
- 黄素治疗促进了膀癌细胞的亡.
结论:
- 黄素有效地抑制了膀癌的进展.
- AKT/MMP14信号通路是黄素抗癌作用的关键调解者.
- 黄素通过AKT/MMP14通路向侵袭,证明了膀癌的治疗潜力.
相关概念视频
mTOR Signaling and Cancer Progression
3.8K
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...
3.8K
Drugs that Stabilize Microtubules
2.0K
Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
2.0K
Inhibition of Cdk Activity
4.8K
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...
4.8K


