在分散型大B细胞淋巴瘤中,Plumbagin通过调节ROS-PI3K-Akt-mTOR信号通路来诱导亡
Jingfang Du1, Tao Ye1, Pian Li1
1Hebei University of Engineering School of Clinical Medicine, Handan, Hebei, China.
Critical reviews in eukaryotic gene expression
|February 17, 2025
概括
普伦巴根有效地抑制扩散性大B细胞淋巴瘤 (DLBCL) 细胞增殖,并通过增加活性氧物种 (ROS) 和抑制PI3K/Akt/mTOR通路促进细胞亡,显示出治疗潜力.
科学领域:
- 在瘤学瘤学.
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 扩散性大B细胞淋巴瘤 (DLBCL) 是一种侵略性的非霍奇金淋巴瘤.
- 需要针对DLBCL扩散和亡的新型治疗策略.
- 素 (PL) 是一种具有潜在抗癌性能的天然化合物.
研究的目的:
- 为了研究plumbagin (PL) 对SU-DHL-4细胞 (DLBCL细胞系) 的作用.
- 阐明PL作用的基本机制,包括其对增殖,亡,活性氧物种 (ROS) 和PI3K/Akt/mTOR通路的影响.
- 在老鼠异种移植模型中评估PL的治疗疗效.
主要方法:
- 在体外研究中,使用不同PL度的SU-DHL-4细胞进行治疗.
- 细胞增殖的CCK8测定,细胞亡的流动细胞计和ROS水平.
- 对抗氧化酶活性进行定量实时PCR (qRT-PCR).
- 在关键蛋白质表达 (Bax,Bcl-2,caspase-3,PI3K/Akt/mTOR通路蛋白质) 方面进行西式涂抹.
- 使用老鼠异种移植模型进行体内研究.
主要成果:
- 在时间和剂量上,PL显著抑制了SU-DHL-4细胞增殖并诱导了细胞亡.
- PL治疗增加了ROS的产生,并提高了Bax的调节,并分裂了caspase-3的表达.
- PL降低了Bcl-2,p-PI3K,p-Akt和p-mTOR蛋白质的表达.
- 在老鼠异种移植模型中,PL显示出显著的瘤生长抑制.
结论:
- 普伦巴在DLBCL细胞上表现出抗增殖和促的作用.
- PL的机制涉及ROS上调和PI3K/Akt/mTOR信号通路的抑制.
- 普伦巴金作为DLBCL治疗的潜在治疗剂显示出希望.
更多相关视频
07:15Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
335
06:12Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
Published on: May 3, 2024
1.6K
相关概念视频
The Intrinsic Apoptotic Pathway
6.1K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.1K
PI3K/mTOR/AKT Signaling Pathway
3.4K
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...
3.4K
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
The JAK-STAT Signaling Pathway
8.6K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
8.6K
The Extrinsic Apoptotic Pathway
6.0K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.0K
Abnormal Proliferation
4.4K
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...
4.4K
