鲁II光动力疗法通过准PI3K/AKT/p53信号,抑制非功能性垂体腺瘤的生长
Dong Fan1,2, Zhongyu Wang1,2, Xingyi Yuan1,2
1Department of Neurosurgery, The First Affiliated Hospital, Guangdong Pharmaceutical University, Guangzhou 510699, China.
ACS applied bio materials
|July 17, 2025
概括
使用Ru2的光动力学治疗激活了p53通路,并抑制了非功能性垂体腺瘤 (NFPA) 中的PI3K/AKT信号传递. 这种机制为NFPA治疗提供了一个新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 生物化学 生物化学
- 摄影化学的使用.
背景情况:
- 非功能性垂体腺瘤 (NFPA) 是常见的内瘤,治疗选择有限.
- 目前的手术和放射治疗等治疗方法具有很高的复发率和副作用.
- 光动力学疗法 (PDT) 提供一种局部治疗方法,具有时空控制.
研究的目的:
- 研究NFPA中的光敏剂Ru2的作用机制.
- 阐明受Ru2介导PDT影响的分子标和途径.
主要方法:
- 合成的光敏剂 [Ru(tpy) ((tpy-Br) ](PF6) 2 (Ru2). 这种光敏剂的合成.
- 使用CCK-8测定和活死染色的细胞活力的评估.
- RNA测序 (RNA-seq) 用于识别差异表达的基因.
- 定量PCR (qPCR) 和西斑用于分析PI3K/AKT/p53通路表达.
- 使用PI3K/AKT激动剂的验证和3D多细胞瘤球体 (MCTS) 的评估.
主要成果:
- Ru2-PDT特别激活p53通路,并抑制NFPA细胞 (PDFS) 中的PI3K/AKT酸化.
- 在595nm照明下,Ru2-PDT通过p53激活诱导G0/G1细胞周期停止.
- Ru2-PDT显著抑制PI3K/AKT信号通路的酸化.
- 治疗PI3K/AKT激动剂部分逆转Ru2-PDT的影响,包括减少细胞亡和恢复细胞迁移/侵入.
结论:
- Ru2-PDT的目标是NFPA中的PI3K/AKT/p53信号轴.
- 这项研究为Ru2-PDT作为NFPA的潜在临床治疗提供了机制基础.
相关概念视频
Abnormal Proliferation
4.6K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.6K
PI3K/mTOR/AKT Signaling Pathway
4.0K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
4.0K
mTOR Signaling and Cancer Progression
3.9K
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...
3.9K
Inhibition of Cdk Activity
4.9K
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...
4.9K
Experimental RNAi
6.3K
RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
6.3K
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
257
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
257


