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Published on: October 24, 2015
Abnormal expression and mechanism of miR-330-3p/BTG1 axis in hepatocellular carcinoma
1Department of Clinical Laboratory, Ming Zhou Hospital of Zhejiang University, Ningbo, China. zhaoxing1918@163.com.
Objective:
Increasing evidence has suggested that microRNAs (miRNAs) played critical roles in cancer development by acting as a tumor suppressor or tumor-promoting genes. However, the role of microRNA-330-3p (miR-330-3p) in hepatocellular carcinoma (HCC) is still unknown. This study aimed to investigate the expression and role of miR-330-3p in hepatocarcinogenesis.
Patients And Methods:
A total of 30 human hepatocellular carcinoma tissues and adjacent normal tissues were obtained from 30 hepatocellular carcinoma patients. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was carried out to measure the expression of miR-330-3p in HCC tissues and cell lines. The relation between B-cell translocation gene 1 (BTG1) and miR-330-3p was predicted by TargetScan and confirmed by dual-luciferase reporter assay. Cell Counting Kit-8 (CCK-8), flow cytometry analysis, and transwell assay were used to determine cell viability, apoptosis, cell migration, and invasion, respectively. In addition, the mRNA and protein expression of Cyclin D1, Bcl-2, Bax, and matrix metalloproteinase (MMP)9 were detected using qRT-PCR and Western blotting.
Results:
We found that miR-330-3p expression was up-regulated in HCC tissues and cell lines. BTG1 was a direct target of miR-330-3p and it was down-regulated in HCC tissues and cell lines. Moreover, down-regulation of miR-330-3p suppressed HCCLM3 cell viability, migration, invasion, and enhanced cell apoptosis, while the tumor-suppressive effects were reversed by BTG1-siRNA. In addition, miR-330-3p inhibitor decreased the expression of Cyclin D1, Bcl-2, and MMP9 while enhanced the expression of Bax. Meanwhile, BTG1-siRNA led to the opposite effects.
Conclusions:
The data suggested that miR-330-3p acted as a tumor gene in HCC by targeting BTG1 and it might be a potential therapeutic target for the HCC treatment.
Insights
MicroRNA-330-3p (miR-330-3p) is upregulated in hepatocellular carcinoma (HCC), promoting tumor growth by targeting BTG1. Inhibiting miR-330-3p may offer a new therapeutic strategy for HCC.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) are crucial regulators in cancer development.
- The specific role of microRNA-330-3p (miR-330-3p) in hepatocellular carcinoma (HCC) remains largely uncharacterized.
- Understanding novel miRNA roles is vital for advancing cancer diagnostics and therapeutics.
Purpose of the Study:
- To elucidate the expression profile of miR-330-3p in HCC.
- To investigate the functional role of miR-330-3p in hepatocarcinogenesis.
- To identify potential molecular targets of miR-330-3p in HCC.
Main Methods:
- Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) for miRNA and mRNA expression analysis.
- Dual-luciferase reporter assay to confirm direct targeting of B-cell translocation gene 1 (BTG1) by miR-330-3p.
- Cell proliferation (CCK-8), apoptosis (flow cytometry), migration, and invasion assays (Transwell) to assess functional roles.
Main Results:
- miR-330-3p was significantly upregulated in HCC tissues and cell lines compared to normal controls.
- BTG1 was identified as a direct target of miR-330-3p and was found to be downregulated in HCC.
- Downregulation of miR-330-3p inhibited HCC cell viability, migration, and invasion, while promoting apoptosis, effects reversed by BTG1 knockdown.
Conclusions:
- miR-330-3p functions as an oncogene in HCC by targeting BTG1.
- miR-330-3p represents a potential therapeutic target for hepatocellular carcinoma treatment.
- Targeting the miR-330-3p/BTG1 axis may offer a novel strategy for HCC intervention.
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