微RNA-450b-5p调节的RPLP0通过激活JAK/STAT3通路促进肝细胞癌的进展

相关实验视频

Updated: Jun 11, 2025

07:39

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Yanqiu Meng¹, Xianbin Huang¹, Guangxin Zhang¹

¹Department of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, PR China.

Translational oncology

|October 9, 2024

概括

核糖体蛋白侧面子子单元P0 (RPLP0) 的高表达表明肝细胞癌 (HCC) 的预后不佳. 针对miR-450b-5p/RPLP0/JAK/STAT3通路可能为HCC提供新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生化学

背景情况:

肝细胞癌 (HCC) 由于其潜伏性质,治疗困难和预后不佳而带来了重大临床挑战.
核糖体蛋白侧干子单元P0 (RPLP0) 已被认可为其参与各种瘤进展过程,但其在HCC中的具体作用在很大程度上仍未被定义.

研究的目的:

调查RPLP0在肝细胞癌中的表达,诊断和预后意义.
阐明RPLP0在HCC进展中的调节机制及其作为治疗点的潜力.

主要方法:

在HCC组织中对RPLP0表达的定量分析.
使用曲线下的面积 (AUC) 评估诊断准确性.
预后分析将RPLP0水平与总生存期 (OS) 和无进展区间 (PFI) 相关联.
在体外和体内实验中评估RPLP0在HCC细胞行为和瘤生长中的功能作用.
研究miR-450b-5p和RPLP0之间的调控关系及其对JAK/STAT3信号通路的影响.

主要成果:

在HCC组织中,RPLP0显著上调,显示出高诊断能力 (AUC = 0.908).
升高的RPLP0表达作为一个独立的预后因素,与较差的OS和PFI相关.
低调RPLP0抑制HCC细胞的增殖,克隆性,入侵,迁移和异种移植瘤的生长,同时促进亡.
微RNA-450b-5p直接准并降低RPLP0,导致抑制JAK/STAT3通路.

结论:

RPLP0作为HCC的致癌因子,具有显著的诊断和预后价值.
miR-450b-5p/RPLP0/JAK/STAT3轴代表了HCC进展中的关键调节途径.
准这一轴对开发肝细胞癌的新疗法有相当大的潜力.

关键词:

肝细胞癌 (HCC) 是一种肝细胞癌.JAK/STAT3 这样就好了.核糖体蛋白侧茎子单位P0 (RPLP0)在 miR-450b-5p 中使用.

相关概念视频

01:20

The JAK-STAT Signaling Pathway

8.7K

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...

8.7K

01:22

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

03:03

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...

3.8K

01:07

MAPK Signaling Cascades

5.2K

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

5.2K

02:23

Abnormal Proliferation

4.5K

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...