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Propofol suppresses proliferation and invasion of glioma cells by upregulating microRNA-218 expression.

Xu J, Xu W, Zhu J - Mol Med Rep (2015)

Bottom Line: Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent.In addition, treatment with propofol efficiently reduced MMP‑2 protein expression levels, and overexpression of miR‑218 also decreased MMP‑2 protein expression levels.Whereas, neutralization of miR‑218 using the anti‑miR-218 antibody reversed the effects of propofol on the biological behavior of U373 cells, and on the inhibition of MMP-2 protein expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Jinhua Municipal Central Hospital, Jinhua, Zhejiang 321000, P.R. China.

ABSTRACT
Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent. The present study aimed to assess the effect of propofol on the proliferation and invasion of human glioma cells, and to determine the potential underlying molecular mechanisms. The effects of propofol on U373 glioblastoma cell proliferation, apoptosis and invasion were detected by an MTT assay, caspase‑3 activity measurement and a Matrigel™ invasion assay, respectively. MicroRNA (miR)‑218 expression and matrix metalloproteinase (MMP)‑2 protein expression levels were analyzed by quantitative polymerase chain reaction and western blot analysis, respectively. In addition, miR‑218 precursor was transfected into the cells to assess whether overexpression of miR‑218 could affect MMP‑2 expression. Anti‑miR‑218 was transfected into the cells to evaluate the role of miR‑218 in the effects of propofol on the biological behavior of glioma cells. The results of the present study demonstrated that propofol significantly increased the expression levels of miR‑218, inhibited U373 cell proliferation and invasion, and facilitated apoptosis. In addition, treatment with propofol efficiently reduced MMP‑2 protein expression levels, and overexpression of miR‑218 also decreased MMP‑2 protein expression levels. Whereas, neutralization of miR‑218 using the anti‑miR-218 antibody reversed the effects of propofol on the biological behavior of U373 cells, and on the inhibition of MMP-2 protein expression. In conclusion, propofol may effectively suppress proliferation and invasion, and induce the apoptosis of glioma cells, at least partially through upregulation of miR-218 expression.

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Anti-microRNA (miR)-218 can reverse the effect of propofol. (A) Reverse transcription-quantitative polymerase chain reaction showed decreased miR-218 expression after anti-miR-218 transfection. (B) An MTT assay indicated that anti-miR-218 enhanced U373 cell proliferation following treatment with 5 μg/ml propofol. (C) Hoechst 33258 staining and (D) caspase-3 activity measurement showed suppressed cell apoptosis after anti-miR-218 transfection in U373 cells pretreated with 5 μg/ml propofol. (E) Matrigel invasion assay showed increased invasion of U373 cells after anti-miR-218 transfection. (F) Western blot analysis indicated that anti-miR-218 significantly increased matrix metalloproteinase-2 (MMP-2) protein expression in U373 cells after propofol treatment. *P<0.01, compared with the untreated control group; #P<0.01, compared with propofol-treated group transfected with negative control.
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f5-mmr-12-04-4815: Anti-microRNA (miR)-218 can reverse the effect of propofol. (A) Reverse transcription-quantitative polymerase chain reaction showed decreased miR-218 expression after anti-miR-218 transfection. (B) An MTT assay indicated that anti-miR-218 enhanced U373 cell proliferation following treatment with 5 μg/ml propofol. (C) Hoechst 33258 staining and (D) caspase-3 activity measurement showed suppressed cell apoptosis after anti-miR-218 transfection in U373 cells pretreated with 5 μg/ml propofol. (E) Matrigel invasion assay showed increased invasion of U373 cells after anti-miR-218 transfection. (F) Western blot analysis indicated that anti-miR-218 significantly increased matrix metalloproteinase-2 (MMP-2) protein expression in U373 cells after propofol treatment. *P<0.01, compared with the untreated control group; #P<0.01, compared with propofol-treated group transfected with negative control.

Mentions: The role of miR-218 in the effects of propofol was further explored in U373 cells. Transfection of the cells with anti-miR-218 antibody was performed to knockdown miR-218 expression. The anti-miR-218 antibody significantly reduced miR-218 expression levels, suggesting the successful introduction of anti-miR-218 into the U373 cells (Fig. 5A). Furthermore, transfection with the anti-miR-218 antibody significantly reversed the inhibition of cell proliferation and invasion, and facilitation of apoptosis caused by propofol (Fig. 5B–E). In addition, the inhibitory effects of propofol on the protein expression levels of MMP-2 were markedly neutralized following transfection of the U373 cells with anti-miR-218 (Fig. 5F).


Propofol suppresses proliferation and invasion of glioma cells by upregulating microRNA-218 expression.

Xu J, Xu W, Zhu J - Mol Med Rep (2015)

Anti-microRNA (miR)-218 can reverse the effect of propofol. (A) Reverse transcription-quantitative polymerase chain reaction showed decreased miR-218 expression after anti-miR-218 transfection. (B) An MTT assay indicated that anti-miR-218 enhanced U373 cell proliferation following treatment with 5 μg/ml propofol. (C) Hoechst 33258 staining and (D) caspase-3 activity measurement showed suppressed cell apoptosis after anti-miR-218 transfection in U373 cells pretreated with 5 μg/ml propofol. (E) Matrigel invasion assay showed increased invasion of U373 cells after anti-miR-218 transfection. (F) Western blot analysis indicated that anti-miR-218 significantly increased matrix metalloproteinase-2 (MMP-2) protein expression in U373 cells after propofol treatment. *P<0.01, compared with the untreated control group; #P<0.01, compared with propofol-treated group transfected with negative control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4581763&req=5

f5-mmr-12-04-4815: Anti-microRNA (miR)-218 can reverse the effect of propofol. (A) Reverse transcription-quantitative polymerase chain reaction showed decreased miR-218 expression after anti-miR-218 transfection. (B) An MTT assay indicated that anti-miR-218 enhanced U373 cell proliferation following treatment with 5 μg/ml propofol. (C) Hoechst 33258 staining and (D) caspase-3 activity measurement showed suppressed cell apoptosis after anti-miR-218 transfection in U373 cells pretreated with 5 μg/ml propofol. (E) Matrigel invasion assay showed increased invasion of U373 cells after anti-miR-218 transfection. (F) Western blot analysis indicated that anti-miR-218 significantly increased matrix metalloproteinase-2 (MMP-2) protein expression in U373 cells after propofol treatment. *P<0.01, compared with the untreated control group; #P<0.01, compared with propofol-treated group transfected with negative control.
Mentions: The role of miR-218 in the effects of propofol was further explored in U373 cells. Transfection of the cells with anti-miR-218 antibody was performed to knockdown miR-218 expression. The anti-miR-218 antibody significantly reduced miR-218 expression levels, suggesting the successful introduction of anti-miR-218 into the U373 cells (Fig. 5A). Furthermore, transfection with the anti-miR-218 antibody significantly reversed the inhibition of cell proliferation and invasion, and facilitation of apoptosis caused by propofol (Fig. 5B–E). In addition, the inhibitory effects of propofol on the protein expression levels of MMP-2 were markedly neutralized following transfection of the U373 cells with anti-miR-218 (Fig. 5F).

Bottom Line: Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent.In addition, treatment with propofol efficiently reduced MMP‑2 protein expression levels, and overexpression of miR‑218 also decreased MMP‑2 protein expression levels.Whereas, neutralization of miR‑218 using the anti‑miR-218 antibody reversed the effects of propofol on the biological behavior of U373 cells, and on the inhibition of MMP-2 protein expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Jinhua Municipal Central Hospital, Jinhua, Zhejiang 321000, P.R. China.

ABSTRACT
Propofol (2,6-diisopropylphenol) is a commonly used intravenous anesthetic agent. The present study aimed to assess the effect of propofol on the proliferation and invasion of human glioma cells, and to determine the potential underlying molecular mechanisms. The effects of propofol on U373 glioblastoma cell proliferation, apoptosis and invasion were detected by an MTT assay, caspase‑3 activity measurement and a Matrigel™ invasion assay, respectively. MicroRNA (miR)‑218 expression and matrix metalloproteinase (MMP)‑2 protein expression levels were analyzed by quantitative polymerase chain reaction and western blot analysis, respectively. In addition, miR‑218 precursor was transfected into the cells to assess whether overexpression of miR‑218 could affect MMP‑2 expression. Anti‑miR‑218 was transfected into the cells to evaluate the role of miR‑218 in the effects of propofol on the biological behavior of glioma cells. The results of the present study demonstrated that propofol significantly increased the expression levels of miR‑218, inhibited U373 cell proliferation and invasion, and facilitated apoptosis. In addition, treatment with propofol efficiently reduced MMP‑2 protein expression levels, and overexpression of miR‑218 also decreased MMP‑2 protein expression levels. Whereas, neutralization of miR‑218 using the anti‑miR-218 antibody reversed the effects of propofol on the biological behavior of U373 cells, and on the inhibition of MMP-2 protein expression. In conclusion, propofol may effectively suppress proliferation and invasion, and induce the apoptosis of glioma cells, at least partially through upregulation of miR-218 expression.

Show MeSH
Related in: MedlinePlus