相关实验视频

Updated: May 12, 2025

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

在肝细胞癌中,MiR-22/GLUT1轴诱导代谢重编程和sorafenib抵抗

Ilaria Leoni^1,2, Giuseppe Galvani^1,2, Elisa Monti^1,2

¹Department for Life Quality Studies, University of Bologna, 47921 Rimini, Italy.

International journal of molecular sciences

|May 7, 2025

概括

微RNA-22 (miR-22) 下调促进肝细胞癌 (HCC) 的攻击性和 sorafenib 耐药性,通过准 GLUT1.1. 循环中的miR-22水平可以预测患者对索拉费尼布治疗的反应.

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:

免疫疗法已经改变了肝细胞癌 (HCC) 治疗方法.
索拉费尼布是高级HCC的关键一线疗法,但获得的耐药性限制了其有效性.
预测生物标志物对于优化HCC患者索拉芬尼治疗至关重要.

研究的目的:

研究微RNA-22 (miR-22) 在HCC.内代谢重编程中的作用.
探索miR-22作为HCC中索拉费尼布反应预测生物标志物的潜力.
为了阐明miR-22/GLUT1轴在HCC进展和耐药性中的作用.

主要方法:

定量PCR (qPCR) 用于分析HCC组织和模型中的miR-22表达.
在HCC细胞中进行功能测试,以评估GLUT1作为直接的miR-22点.
细胞和代谢测试以评估miR-22/GLUT1轴对瘤行为和索拉芬尼布反应的影响.
在HCC患者和接受sorafenib治疗的老鼠中分析循环miR-22.

主要成果:

发现MiR-22在HCC下调,与侵袭性瘤特征相关.
通过向GLUT1.1,MiR-22调节HIF1A通路,增强细胞生存,促进糖分解,并通过向GLUT1.1,增加索拉芬尼抗性.
在HCC患者和临床前模型中,高血清miR-22水平与sorafenib耐药性有关.
在临床前研究中,GLUT1抑制使具有低miR-22表达的HCC细胞对sorafenib敏感.

结论:

循环中的miR-22显示为HCC中索拉费尼布反应的预测生物标志物具有前途.
向GLUT1,特别是在高循环miR-22的患者中,可能是一个可行的治疗策略,可以与sorafenib结合使用.

关键词:

这就是 GLUT1 的原因.在HCC中,HCC是HCC.这就是miR-22的原因.索拉芬尼布 (Sorafenib) 是一个

更多相关视频

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Published on: October 23, 2018

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

相关概念视频

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...

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...