相关实验视频

Updated: Jul 23, 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

过度表达AKR1C1导致在肝细胞癌中产生伦瓦提尼布耐药性

Cheng Gao¹, Liang Chang¹, Tianxin Xu¹

¹Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, China.

Journal of gastrointestinal oncology

|July 12, 2023

概括

伦瓦丁尼布抑制肝细胞癌 (HCC) 细胞增殖. 过高的阿尔多基托减少酶家族1成员C1 (AKR1C1) 表达与伦瓦提尼布耐药性有关,这表明AKR1C1是肝癌的潜在治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
基因组学就是基因组学.

背景情况:

伦瓦提尼布是一种已批准用于肝细胞癌 (HCC) 的多向氨酸激酶抑制剂.
了解伦瓦替尼的点和HCC的耐药性机制对于优化治疗至关重要.
目前关于HCC中伦瓦提尼布耐药性的知识有限.

研究的目的:

为了研究在HCC. lenvatinib耐药性背后的分子机制.
为了确定克服伦瓦替尼布耐药性的潜在治疗点.
探索AKR1C1和miR-4644在伦瓦替尼治疗的HCC中的作用.

主要方法:

使用细胞增殖试验 (殖民地形成,EDU,伤口愈合,CCK-8) 和异种移植瘤模型.
RNA测序 (RNA-seq) 分析了伦瓦提尼布治疗的HCC细胞中的转录组变化.
生物信息分析预测了蛋白质相互作用,KEGG通路,免疫细胞比例 (CIBERSORT) 和miRNA目标.

主要成果:

伦瓦提尼布治疗抑制了HCC细胞的增殖.
在抗伦瓦丁尼布 (LR) HCC 细胞系和组织中观察到AKR1C1表达的增加.
MicroRNA 4644 (miR-4644) 被确定为早期检测伦瓦提尼布耐药性的潜在生物标志物.

结论:

AKR1C1可能是患有伦瓦替尼布抗性HCC的患者的新疗法标.
在LR细胞中发现了免疫微环境和药物敏感性的显著变化.
对AKR1C1和miR-4644的进一步研究可能会导致改善HCC治疗策略.

关键词:

阿尔多-基因减少酶家族1成员C1 (AKR1C1)生物标志物生物标志物药物敏感性药物敏感性肝细胞癌 (HCC) 是一种肝细胞癌.伦瓦提尼布耐药性伦瓦提尼布耐药性

更多相关视频

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Published on: June 26, 2019

A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma

A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma

Published on: September 30, 2021

相关概念视频

Treatment Resistant Cancers

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

Combination Therapies and Personalized Medicine

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

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...