相关实验视频

Updated: Sep 18, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

AP1S3通过调节PI3K/AKT/mTOR通路来影响乳腺癌细胞中的脂质代谢

Zankai Wu¹, Shanshan Wang², Qingfeng Yang¹

¹Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China.

Biochemical and biophysical research communications

|June 24, 2025

概括

适配蛋白复合体1西格玛3 (AP1S3) 通过增强脂质代谢和激活PI3K/AKT/mTOR通路,促进乳腺癌的进展. 向AP1S3为转移性乳腺癌提供了潜在的新疗法.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

乳腺癌 (BRCA) 仍然是全球癌症相关死亡的主要原因.
了解推动BRCA进展的分子机制对于开发有效疗法至关重要.
异常的脂质代谢和信号通路在癌症发展中越来越被认可.

研究的目的:

研究适应蛋白复合体1西格玛3 (AP1S3) 在乳腺癌进展中的作用.
阐明AP1S3对脂质代谢和BRCA中的PI3K/AKT/mTOR信号通路的影响.
评估AP1S3作为转移性乳腺癌的潜在治疗点.

主要方法:

在BRCA中使用TCGA数据进行AP1S3表达分析.
基因本体学 (GO) 和KEGG通路分析.
在体外测试 (CCK-8,殖民地形成,伤口愈合,Transwell) 来评估细胞增殖和迁移.
测量脂质滴积累,自由脂肪酸 (FFA) 和总胆固醇 (TC) 水平.

主要成果:

在BRCA中AP1S3被显著上调,并与预后不佳有关.
AP1S3的淘汰抑制了BRCA细胞的增殖和迁移.
通过PI3K/AKT/mTOR通路的激活,AP1S3促进脂质代谢和瘤进展.
AP1S3沉默降低了脂质积累,并降低了脂质代谢基因的调节.

结论:

通过调节脂质代谢和PI3K/AKT/mTOR通路,AP1S3在BRCA进展中发挥着关键作用.
AP1S3代表了转移性乳腺癌的一个有前途的治疗点.
针对AP1S3可能为BRCA患者提供新的治疗策略.

关键词:

AP1S3 AP1S3 AP1S3 AP1S3 AP1S3 AP1S3 AP1 乳腺癌是什么? 乳腺癌是什么脂质新陈代谢脂质新陈代谢在PI3K/AKT/mTOR路径中.

更多相关视频

Phospholipid Mediator Induced Transformation in Three-Dimensional Cultures

Phospholipid Mediator Induced Transformation in Three-Dimensional Cultures

Published on: July 27, 2022

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

相关概念视频

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

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...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

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 JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

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...

Phosphoinositides and PIPs

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...

Abnormal Proliferation

Abnormal Proliferation

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...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

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...