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Updated: Mar 22, 2026

Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy
Published on: April 29, 2014
MiR-144 inhibits cell proliferation of renal cell carcinoma by targeting MTOR
Cheng Xiang1, Shi-Peng Cui2, You Ke3
1Department of General Surgery, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Abstract:
MicroRNAs (miRNAs) modulate the expression of tumorigenesis-related genes and play important roles in the development of various types of cancers. It has been reported that miR-144 is dysregulated and involved in multiple malignant tumors, but its role in renal cell carcinoma (RCC) remains elusive. In this study, we demonstrated miR-144 was significantly downregulated in human RCC. The decreased miR-144 correlated with tumor size and TNM stage. Moreover, overexpression of miR-144 in vitro suppressed RCC cell proliferation and G2 transition, which were reversed by inhibition of miR-144. Bioinformatic analysis predicted that mTOR was a potential target of miR-144, which was further confirmed by dual luciferase reporter assay. Additionally, the examination of clinical RCC specimens revealed that miR-144 was inversely related to mTOR. Furthermore, knocking down mTOR with siRNA had the same biological effects as those of miR-144 overexpression in RCC cells, including cell proliferation inhibition and S/G2 cell cycle arrest. In conclusion, our results indicate that miR-144 affects RCC progression by inhibiting mTOR expression, and targeting miR-144 may act as a novel strategy for RCC treatment.
Insights
MicroRNA-144 (miR-144) is downregulated in renal cell carcinoma (RCC), inhibiting tumor growth by targeting mTOR. Restoring miR-144 levels offers a potential new treatment strategy for RCC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) regulate genes involved in cancer development.
- miR-144 is implicated in various cancers, but its role in renal cell carcinoma (RCC) is unclear.
Purpose of the Study:
- To investigate the role and mechanism of miR-144 in renal cell carcinoma (RCC).
Main Methods:
- Quantified miR-144 levels in RCC tissues and cell lines.
- Overexpressed/inhibited miR-144 in vitro and assessed effects on cell proliferation and cell cycle.
- Utilized bioinformatic analysis and dual luciferase reporter assays to identify and validate miR-144 targets.
- Knocked down potential target mTOR using siRNA.
Main Results:
- miR-144 was significantly downregulated in human RCC, correlating with tumor size and TNM stage.
- miR-144 overexpression suppressed RCC cell proliferation and G2 transition; inhibition reversed these effects.
- mTOR was identified as a direct target of miR-144, with inverse expression in clinical RCC specimens.
- Knocking down mTOR mimicked the anti-proliferative and cell cycle arrest effects of miR-144 overexpression.
Conclusions:
- miR-144 suppresses RCC progression by inhibiting mTOR expression.
- Targeting miR-144 presents a potential novel therapeutic strategy for renal cell carcinoma.
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