菲科林3通过降低IR/SREBP轴介导的MUFA合成来促进HCC中的铁亡
Yanmei Yuan1, Junting Xu1, Quanxin Jiang1
1Shanghai Diabetes Institute, Department of Endocrinology and Metabolism, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
概括
菲科林3 (FCN3) 向胰岛素受体信号,以减少单不和脂肪酸,增强肝癌中铁灭的敏感性. 这一发现为肝细胞癌 (HCC) 治疗提供了新的策略.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 铁亡是癌症治疗的关键目标.
- 单不和脂肪酸 (MUFA) 抑制铁亡.
- 补充系统蛋白 Ficolin 3 (FCN3) 显示出瘤抑制作用,但其在脂质代谢和铁亡中的作用尚不清楚.
研究的目的:
- 为了研究Ficolin 3 (FCN3) 在调节脂肪代谢和肝细胞癌 (HCC) 中的ferroptosis中的作用.
- 阐明FCN3在HCC中的作用的基础分子机制.
主要方法:
- 使用细胞活力,BODIPY-C11染色和MDA试验评估铁灭.
- 使用初级HCC和异种移植模型进行体内研究.
- 进行了代谢分析,以评估脂质水平的变化.
主要成果:
- 降低FCN3表达与HCC中的MUFA积累和铁衰抵抗相关.
- 过度表达的FCN3使HCC细胞对铁亡敏感,从而抑制瘤的进展.
- 通过抑制亲IR裂变和酸化,FCN3通过抑制SREBP1c介导的脂质生成和MUFA合成,使胰岛素受体β (IR-β) 失活.
结论:
- 通过IR-β/SREBP1c通路,FCN3增强了HCC细胞对铁亡的敏感性.
- 准FCN3诱导的铁亡是一种新的治疗策略,用于HCC.
更多相关视频
09:21Ferritinophagy: Assessing the Selective Degradation of Iron by Autophagy in Human Fibroblasts
Published on: February 23, 2024
897
08:04Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
Published on: October 23, 2018
18.9K
相关概念视频
Necrosis
4.5K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.5K
Receptor Downregulation in MVBs
2.1K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
2.1K
NF-κB-dependent Signaling Pathway
7.4K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.4K
