Related Experiment Video
Updated: Feb 22, 2026
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-122 promotes metastasis of clear-cell renal cell carcinoma by downregulating Dicer
Yang Fan1, Xin Ma1, Hongzhao Li1
1State Key Laboratory of Kidney Diseases, Department of Urology, Chinese People's Liberation Army General Hospital, PLA Medical School, Beijing, People's Republic of China.
Abstract:
Although overall downregulation of microRNAs (miRNAs) is a general feature of clear-cell renal cell carcinoma (ccRCC), several miRNAs are consistently upregulated, among which miR-122 was markedly increased in ccRCC tissues. Our study aims to determine the functional importance and underlying mechanism of miR-122 in ccRCC metastasis. Here, we demonstrate that the expression of miR-122 increased in ccRCC tissues, and higher miR-122 expression was found in ccRCC tissues with metastatic disease than in those without metastasis. The increased miR-122 levels were associated with poor metastasis-free survival in ccRCC patients with localized disease. Dicer was validated as a direct functional target of miR-122. Overexpression of miR-122 promoted migration and invasion of ccRCC cells in vitro and metastatic behavior of ccRCC cells in vivo. Inhibition of miR-122 attenuated this metastatic phenotype in vitro. Importantly, miR-122 exerted its pro-metastatic properties in ccRCC cells by downregulating Dicer and its downstream effector, the miR-200 family, thereby inducing epithelial-mesenchymal transition (EMT). Our results suggest an important role of the miR-122/Dicer/miR-200s/EMT pathway in ccRCC metastasis. Furthermore, miR-122 may serve as a biomarker for discriminating ccRCC with metastatic potential.
Insights
MicroRNA-122 (miR-122) is upregulated in clear-cell renal cell carcinoma (ccRCC) and promotes metastasis by downregulating Dicer and the miR-200 family, inducing epithelial-mesenchymal transition (EMT). This pathway highlights miR-122 as a potential biomarker for ccRCC metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are generally downregulated in clear-cell renal cell carcinoma (ccRCC).
- However, specific miRNAs, including miR-122, are notably upregulated in ccRCC tissues.
- Elevated miR-122 expression correlates with metastatic ccRCC and poorer patient survival.
Purpose of the Study:
- To investigate the functional role and molecular mechanisms of miR-122 in ccRCC metastasis.
- To determine if miR-122 can serve as a biomarker for metastatic potential in ccRCC.
Main Methods:
- Quantitative analysis of miR-122 expression in ccRCC tissues.
- In vitro and in vivo experiments assessing the effects of miR-122 overexpression and inhibition on ccRCC cell migration, invasion, and metastasis.
- Validation of Dicer as a direct target of miR-122.
- Analysis of the miR-122/Dicer/miR-200 family/epithelial-mesenchymal transition (EMT) pathway.
Main Results:
- miR-122 expression is significantly increased in ccRCC tissues, particularly in those with metastasis.
- Higher miR-122 levels are associated with reduced metastasis-free survival in ccRCC patients.
- Overexpression of miR-122 enhances ccRCC cell migration, invasion, and in vivo metastasis.
- Inhibition of miR-122 suppresses these pro-metastatic phenotypes.
- miR-122 promotes metastasis by downregulating Dicer, which in turn affects the miR-200 family and induces EMT.
Conclusions:
- The miR-122/Dicer/miR-200s/EMT pathway plays a critical role in ccRCC metastasis.
- miR-122 is a key driver of ccRCC cell invasion and metastatic potential.
- miR-122 holds promise as a diagnostic biomarker for identifying ccRCC with metastatic capabilities.
Related Concept Videos
01:22MicroRNAs
01:22MicroRNAs
02:15Experimental RNAi