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Updated: Apr 7, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
MicroRNA‑21 regulates the expression of BTG2 in HepG2 liver cancer cells
Bijing Mao1, He Xiao1, Zhimin Zhang2
1Cancer Center, Institute of Surgical Research, Daping Hospital, Third Military Medical University, Chongqing 400042, P.R. China.
Abstract:
B‑cell translocation gene 2 (BTG2) is a tumor suppressor gene, which belongs to the anti‑proliferation gene family. Our previous study demonstrated that microRNA (miR)‑21 and the expression of BTG2 were negatively correlated during hepatocarcinogenesis. The aim of the present study was to investigate the effects of miR‑21 on the growth and progression of liver cancer cells, and to determine the underlying mechanism. A luciferase reporter assay was used to demonstrate that the BTG2 gene was a direct target of miR‑21. In addition, the effects of miR‑21 on cell growth and gene expression in HepG2 human hepatocellular carcinoma (HCC) cells were analyzed using reverse transcription‑quantitative polymerase chain reaction, western blotting, an MTT assay, flow cytometry, a Transwell invasion assay and a wound healing assay. The expression levels of miR‑21 in the HepG2 cells were significantly higher, compared with those in L02 normal liver cells. The expression levels of BTG2 in liver cancer cell lines (HepG2 and Huh7) were significantly lower, compared with that in the L02 cells. These results suggested that BTG2 was the direct target gene of miR‑21. The protein expression levels of BTG2 were inhibited by high expression levels of miR‑21, and increased by inhibition of the expression of miR‑21 in the HepG2 cells. Inhibition of miR‑21 reduced cell proliferation and invasion, and increased the rate of apoptosis in the HepG2 cells. These results indicated that miR‑21 regulates cell proliferation, invasion, migration and apoptosis in HepG2 cells, which may be associated with its effects on the expression of BTG2. The results of the present study may provide a basis for targeting the miR‑21/BTG2 interaction for the treatment of HCC.
Insights
MicroRNA-21 (miR-21) promotes liver cancer by suppressing the tumor suppressor gene BTG2. Inhibiting miR-21 reduces cancer cell growth, invasion, and increases apoptosis, suggesting miR-21/BTG2 targeting for HCC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Hepatology
Background:
- B-cell translocation gene 2 (BTG2) acts as a tumor suppressor and is part of the anti-proliferation gene family.
- Previous research indicated a negative correlation between microRNA-21 (miR-21) and BTG2 expression during liver cancer development (hepatocarcinogenesis).
Purpose of the Study:
- To investigate the impact of miR-21 on the growth and progression of liver cancer cells.
- To elucidate the underlying molecular mechanism by which miR-21 influences liver cancer.
Main Methods:
- Luciferase reporter assay to confirm BTG2 as a direct target of miR-21.
- Analysis of miR-21 effects on HepG2 cells using RT-qPCR, Western blotting, MTT assay, flow cytometry, Transwell invasion, and wound healing assays.
Main Results:
- miR-21 expression was significantly elevated in HepG2 liver cancer cells compared to normal L02 cells.
- BTG2 expression was significantly reduced in HepG2 and Huh7 liver cancer cells versus L02 cells.
- High miR-21 inhibited BTG2 protein levels, while miR-21 inhibition increased BTG2 expression.
- Inhibition of miR-21 decreased proliferation and invasion, and increased apoptosis in HepG2 cells.
Conclusions:
- miR-21 directly targets BTG2, inhibiting its expression and promoting liver cancer cell proliferation, invasion, and migration.
- The miR-21/BTG2 pathway is a potential therapeutic target for hepatocellular carcinoma (HCC).
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