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MicroRNA‑21 regulates the expression of BTG2 in HepG2 liver cancer cells.

Mao B, Xiao H, Zhang Z, Wang D, Wang G - Mol Med Rep (2015)

Bottom Line: The expression levels of miR‑21 in the HepG2 cells were significantly higher, compared with those in L02 normal liver 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.

View Article: PubMed Central - PubMed

Affiliation: Cancer 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.

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Effects of miR-21 inhibitor on the viability of HepG2 liver cancer cells. *P<0.05, **P<0.01, compared with the NC-transfected cells. Data are presented as the mean ± standard deviation. miR-21, microRNA-21; NC, negative control; OD, optical density.
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f3-mmr-12-04-4917: Effects of miR-21 inhibitor on the viability of HepG2 liver cancer cells. *P<0.05, **P<0.01, compared with the NC-transfected cells. Data are presented as the mean ± standard deviation. miR-21, microRNA-21; NC, negative control; OD, optical density.

Mentions: The present study aimed to further analyze the association between miR-21 and cell growth by comparing the cell viabilities between cells treated with miR-21 inhibitor and NC. The viability of the HepG2 cells transfected with the miR-21 inhibitor was significantly lower, compared with the cells transfected with the NC (P<0.05; Fig. 3).


MicroRNA‑21 regulates the expression of BTG2 in HepG2 liver cancer cells.

Mao B, Xiao H, Zhang Z, Wang D, Wang G - Mol Med Rep (2015)

Effects of miR-21 inhibitor on the viability of HepG2 liver cancer cells. *P<0.05, **P<0.01, compared with the NC-transfected cells. Data are presented as the mean ± standard deviation. miR-21, microRNA-21; NC, negative control; OD, optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581755&req=5

f3-mmr-12-04-4917: Effects of miR-21 inhibitor on the viability of HepG2 liver cancer cells. *P<0.05, **P<0.01, compared with the NC-transfected cells. Data are presented as the mean ± standard deviation. miR-21, microRNA-21; NC, negative control; OD, optical density.
Mentions: The present study aimed to further analyze the association between miR-21 and cell growth by comparing the cell viabilities between cells treated with miR-21 inhibitor and NC. The viability of the HepG2 cells transfected with the miR-21 inhibitor was significantly lower, compared with the cells transfected with the NC (P<0.05; Fig. 3).

Bottom Line: The expression levels of miR‑21 in the HepG2 cells were significantly higher, compared with those in L02 normal liver 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.

View Article: PubMed Central - PubMed

Affiliation: Cancer 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.

Show MeSH
Related in: MedlinePlus