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Updated: Dec 5, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-183-5p contributes to malignant progression through targeting PDCD4 in human hepatocellular carcinoma
Xiaohui Duan1, Wei Li1, Peng Hu1
1Research Laboratory of Hepatobiliary Tumor, Department of Hepatobiliary Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha 410005, China.
Abstract:
Hepatocellular carcinoma (HCC) remains one of the most common malignant tumors worldwide. The present study aimed to investigate the biological role of microRNA-183-5p (miR-183-5p), a novel tumor-related microRNA (miRNA), in HCC and illuminate the possible molecular mechanisms. The expression patterns of miR-183-5p in clinical samples were characterized using qPCR analysis. Kaplan-Meier survival curve was applied to evaluate the correlation between miR-183-5p expression and overall survival of HCC patients. Effects of miR-183-5p knockdown on HCC cell proliferation, apoptosis, migration and invasion capabilities were determined via Cell Counting Kit-8 (CCK8) assays, flow cytometry, scratch wound healing assays and Transwell invasion assays, respectively. Mouse neoplasm transplantation models were established to assess the effects of miR-183-5p knockdown on tumor growth in vivo. Bioinformatics analysis, dual-luciferase reporter assays and rescue assays were performed for mechanistic researches. Results showed that miR-183-5p was highly expressed in tumorous tissues compared with adjacent normal tissues. Elevated miR-183-5p expression correlated with shorter overall survival of HCC patients. Moreover, miR-183-5p knockdown significantly suppressed proliferation, survival, migration and invasion of HCC cells compared with negative control treatment. Consistently, miR-183-5p knockdown restrained tumor growth in vivo. Furthermore, programmed cell death factor 4 (PDCD4) was identified as a direct target of miR-183-5p. Additionally, PDCD4 down-regulation was observed to abrogate the inhibitory effects of miR-183-5p knockdown on malignant phenotypes of HCC cells. Collectively, our data suggest that miR-183-5p may exert an oncogenic role in HCC through directly targeting PDCD4. The current study may offer some new insights into understanding the role of miR-183-5p in HCC.
Insights
MicroRNA-183-5p (miR-183-5p) is highly expressed in hepatocellular carcinoma (HCC) and promotes tumor growth. Targeting miR-183-5p and its target, programmed cell death factor 4 (PDCD4), may offer new therapeutic strategies for HCC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) is a prevalent global malignancy.
- MicroRNAs (miRNAs) play critical roles in cancer development and progression.
- The specific role of microRNA-183-5p (miR-183-5p) in HCC remains largely unexplored.
Purpose of the Study:
- To investigate the biological function of miR-183-5p in HCC.
- To elucidate the underlying molecular mechanisms of miR-183-5p in HCC pathogenesis.
- To evaluate the potential of miR-183-5p as a therapeutic target in HCC.
Main Methods:
- Quantitative PCR (qPCR) for miRNA expression analysis in clinical HCC samples.
- In vitro assays (CCK8, flow cytometry, scratch wound, Transwell) to assess HCC cell behavior.
- In vivo mouse xenograft models for tumor growth evaluation.
- Bioinformatics, dual-luciferase reporter, and rescue assays for mechanistic studies.
Main Results:
- miR-183-5p was significantly upregulated in HCC tissues compared to adjacent normal tissues.
- High miR-183-5p expression correlated with poorer overall survival in HCC patients.
- Knockdown of miR-183-5p inhibited HCC cell proliferation, migration, invasion, and tumor growth in vivo.
- Programmed cell death factor 4 (PDCD4) was identified as a direct target of miR-183-5p.
- PDCD4 downregulation counteracted the inhibitory effects of miR-183-5p knockdown on HCC phenotypes.
Conclusions:
- miR-183-5p acts as an oncogene in hepatocellular carcinoma.
- The oncogenic role of miR-183-5p in HCC is mediated through direct targeting of PDCD4.
- miR-183-5p and its regulatory pathway involving PDCD4 represent potential therapeutic targets for HCC.
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