在三阴性乳腺癌中,miRNA-200c-3p缺陷通过激活CRKL表达来促进表皮层-介质细胞过渡

在三阴性乳腺癌中,miRNA-200c-3p缺陷通过激活CRKL表达来促进表皮层-介质细胞过渡

相关实验视频

Updated: Jun 26, 2025

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.4K

Fangfang Nie¹, Qinfang Zhang¹, WeiNa Ma²

¹Department of Oncology, Jiading District Central Hospital Affiliated Shanghai University of Medicine & Health Sciences, No. 1 Chengbei Road, Jiading District, Shanghai, 201800, China.

Discover oncology

|May 8, 2024

概括

微RNA-200c-3p通过降低CRKL的调节来抑制三阴性乳腺癌 (TNBC) 的进展,CRKL是表皮-介质细胞过渡 (EMT) 中的关键参与者. 这一发现阐明了TNBC恶性瘤的一个关键机制.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

表皮-介质细胞转换 (EMT) 对三阴性乳腺癌 (TNBC) 恶性进展至关重要.
miRNA-200c-3p与EMT有关,但其在TNBC中的确切作用和机制尚不清楚.
CRKL蛋白经常在瘤中过度表达,并导致EMT.

研究的目的:

研究miRNA-200c-3p调节TNBC中EMT的机制.
通过准CRKL.p来确定miRNA-200c-3p是否抑制TNBC恶性瘤.
阐明miRNA-200c-3p/CRKL轴在TNBC进展中的作用.

主要方法:

生物信息分析 (miRPathDB,Targetscan,PicTar,Coremine Medica) 以确定潜在的miRNA标.
实验验证包括RT-PCR,西式斑点,细胞增殖 (CCK-8),入侵 (Transwell) 和克隆形成测试.
使用裸体老鼠异种移植模型的体内研究和体内光酶记者测试.

主要成果:

发现miRNA-200c-3p在TNBC中表达不足,同时对EMT标志物的上调调节.
miRNA-200c-3p显著抑制了TNBC细胞的增殖,入侵和EMT相关的基因/蛋白质表达.
鉴定出CRKL是miRNA-200c-3p的直接标,其被miRNA-200c-3p抑制的抑制抑制了EMT.

结论:

通过抑制EMT,miRNA-200c-3p在TNBC中起到瘤抑制作用.
在TNBC恶性瘤上miRNA-200c-3p的抑制作用是通过CRKL的直接下调调节来调节的.
针对miRNA-200c-3p/CRKL通路为TNBC提供了一个潜在的治疗策略.

关键词:

CRKL CRKL 是一个字.皮质-介质细胞过渡.恶性现象型的恶性现象型.三阴性乳腺癌是三阴性乳腺癌.

更多相关视频

Induction and Analysis of Epithelial to Mesenchymal Transition

10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

35.8K

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

06:54

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

Published on: October 27, 2020

12.9K

相关概念视频

01:22

MicroRNAs

21.3K

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...

21.3K

02:30

Metastasis

5.5K

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

5.5K

01:15

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...

2.1K

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...