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Updated: May 3, 2026
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
Overexpression of miR-126 inhibits the activation and migration of HSCs through targeting CRK
Xu-Hua Gong1, Chao Chen, Peng Hou
1Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Background & Aims:
MicroRNAs (miRNAs) have been shown to play essential roles in HSCs activation which contributes to hepatic fibrosis. Our previous miRNA microarray results suggested that miR-126 might be decreased during HSCs activation as other studies. The aim of this study is to investigate the role of miR-126 during HSCs activation.
Methods:
In this study, the expression of miR-126 during HSCs activation was measured and confirmed by qRT-PCR. Then, miR-126 expression was restored by transfection of lentivirus vector encoding miR-126. Futhermore, cell proliferation was assayed by the cell counting kit-8 (CCK-8), cell migration was assayed by transwell assay, and the markers of activation of HSCs, α-SMA and collagen type I, were assayed by qRT-PCR, Western Blotting, Immunostaining and ELISA. Luciferase reporter assay was used to find the target of miR-126, and Western Blotting and Immunostaining was used to validate the target of miR-126. Then, the expression and the role of the target of miR-126 during HSCs activation was further assessed.
Results:
The expression of miR-126 was confirmed to be significantly decreased during HSCs activation. Overexpression of miR-126 significantly inhibited HSCs migration but did not affect HSCs proliferation. The expression of α-SMA and collagen type I were both obviously decreased by miR-126 restoration. CRK was found to be the target of miR-126 and overexpression of miR-126 significantly inhibited CRK expression. And it was found that overexpression of CRK also significantly decreased miR-126 expression and promoted HSCs activation.
Conclusions:
Our study showed that overexpression of miR-126 significantly inhibited the activation and migration of HSCs through targeting CRK which can also decrease miR-126 expression and promote HSCs activation.
Insights
MicroRNA-126 (miR-126) inhibits hepatic stellate cell (HSC) activation and migration by targeting CRK. Restoring miR-126 levels is a potential therapeutic strategy for hepatic fibrosis.
Area of Science:
- Hepatology
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) regulate hepatic stellate cell (HSC) activation, a key process in hepatic fibrosis.
- Previous studies suggest miR-126 levels decrease during HSC activation.
Purpose of the Study:
- To investigate the role of miR-126 in HSC activation.
- To identify the molecular targets of miR-126 in this process.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure miR-126 expression.
- Lentivirus-mediated restoration of miR-126 in HSCs.
- Assays for cell proliferation (CCK-8), migration (Transwell), and activation markers (α-SMA, collagen type I).
- Luciferase reporter assay to identify and validate miR-126 targets.
Main Results:
- miR-126 expression was significantly decreased in activated HSCs.
- Overexpression of miR-126 inhibited HSC migration and reduced α-SMA and collagen type I expression.
- CRK was identified as a direct target of miR-126; miR-126 overexpression suppressed CRK, while CRK overexpression reduced miR-126 and promoted HSC activation.
Conclusions:
- miR-126 plays a crucial inhibitory role in HSC activation and migration.
- The miR-126/CRK axis is a significant regulator of HSC activation, offering a potential therapeutic target for hepatic fibrosis.
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