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MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway.

Yang TQ, Lu XJ, Wu TF, Ding DD, Zhao ZH, Chen GL, Xie XS, Li B, Wei YX, Guo LC, Zhang Y, Huang YL, Zhou YX, Du ZW - Cancer Sci. (2014)

Bottom Line: MicroRNA-16 decreased glioma malignancy by downregulating NF-κB1 and MMP9, and led to suppressed invasiveness of human glioma cell lines SHG44, U87, and U373.Our results also indicated that upregulation of miR-16 promoted apoptosis by suppressing BCL2 expression.Finally, the upregulation of miR-16 in a nude mice model of human glioma resulted in significant suppression of glioma growth and invasiveness.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.

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MicroRNA-16 (miR-16) directly targets nuclear factor-κB1 (NF-κB1) in human glioma. (a) Analyzing the homology of miR-16 and NF-κB1 mRNA sequences. has-miR-16, Homo sapiens; mmu-miR-16, Mus musculus. (b) Luciferase assay revealed reduced relative luciferase activities in 293T cells stably overexpressing miR-16 following transfection of NF-κB1 3′-UTR using pMIR and pMIR-REPORT vectors. **P < 0.01. FL, firefly luminescence; RL, Renilla luminescence. (c,d) Quantitative RT-PCR and Western blot analysis showed that miR-16 inhibited the expression of NF-κB1. *P < 0.05; **P < 0.01.
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fig02: MicroRNA-16 (miR-16) directly targets nuclear factor-κB1 (NF-κB1) in human glioma. (a) Analyzing the homology of miR-16 and NF-κB1 mRNA sequences. has-miR-16, Homo sapiens; mmu-miR-16, Mus musculus. (b) Luciferase assay revealed reduced relative luciferase activities in 293T cells stably overexpressing miR-16 following transfection of NF-κB1 3′-UTR using pMIR and pMIR-REPORT vectors. **P < 0.01. FL, firefly luminescence; RL, Renilla luminescence. (c,d) Quantitative RT-PCR and Western blot analysis showed that miR-16 inhibited the expression of NF-κB1. *P < 0.05; **P < 0.01.

Mentions: By analyzing the homology between miR-16 and NF-κB1 mRNA sequences, we observed that the 15 nucleotides from the 5′ end of miR-16 were complementary to bases 255–279 of the NF-κB1 cDNA (Homo sapiens, NM_003998 AK122850 M58603; Fig.2a). A dual-luciferase reporter assay system was used to validate whether miR-16 directly recognizes the 3′-UTR region of NF-κB1 mRNA. As shown in Figure2(b), the relative luciferase activities of the pre-miR-16 groups transfected with NF-κB1 3′-UTR constructs were significantly decreased, compared to those transfected with pMIR-NF-κB1 constructs, for the 293T cell line, implying that NF-κB1 is a direct target of miR-16. To further demonstrate the correlation between miR-16 and NF-κB1, mRNA and protein expression of NF-κB1 were detected by qRT-PCR and Western blotting. Data showed that miR-16 upregulation dramatically reduced the protein expression of NF-κB1. Meanwhile, we observed that NF-κB1 expression was increased by downregulating miR-16 (Fig.2c,d). Thus, miR-16 inhibited NF-κB1 expression in human glioma.


MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway.

Yang TQ, Lu XJ, Wu TF, Ding DD, Zhao ZH, Chen GL, Xie XS, Li B, Wei YX, Guo LC, Zhang Y, Huang YL, Zhou YX, Du ZW - Cancer Sci. (2014)

MicroRNA-16 (miR-16) directly targets nuclear factor-κB1 (NF-κB1) in human glioma. (a) Analyzing the homology of miR-16 and NF-κB1 mRNA sequences. has-miR-16, Homo sapiens; mmu-miR-16, Mus musculus. (b) Luciferase assay revealed reduced relative luciferase activities in 293T cells stably overexpressing miR-16 following transfection of NF-κB1 3′-UTR using pMIR and pMIR-REPORT vectors. **P < 0.01. FL, firefly luminescence; RL, Renilla luminescence. (c,d) Quantitative RT-PCR and Western blot analysis showed that miR-16 inhibited the expression of NF-κB1. *P < 0.05; **P < 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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fig02: MicroRNA-16 (miR-16) directly targets nuclear factor-κB1 (NF-κB1) in human glioma. (a) Analyzing the homology of miR-16 and NF-κB1 mRNA sequences. has-miR-16, Homo sapiens; mmu-miR-16, Mus musculus. (b) Luciferase assay revealed reduced relative luciferase activities in 293T cells stably overexpressing miR-16 following transfection of NF-κB1 3′-UTR using pMIR and pMIR-REPORT vectors. **P < 0.01. FL, firefly luminescence; RL, Renilla luminescence. (c,d) Quantitative RT-PCR and Western blot analysis showed that miR-16 inhibited the expression of NF-κB1. *P < 0.05; **P < 0.01.
Mentions: By analyzing the homology between miR-16 and NF-κB1 mRNA sequences, we observed that the 15 nucleotides from the 5′ end of miR-16 were complementary to bases 255–279 of the NF-κB1 cDNA (Homo sapiens, NM_003998 AK122850 M58603; Fig.2a). A dual-luciferase reporter assay system was used to validate whether miR-16 directly recognizes the 3′-UTR region of NF-κB1 mRNA. As shown in Figure2(b), the relative luciferase activities of the pre-miR-16 groups transfected with NF-κB1 3′-UTR constructs were significantly decreased, compared to those transfected with pMIR-NF-κB1 constructs, for the 293T cell line, implying that NF-κB1 is a direct target of miR-16. To further demonstrate the correlation between miR-16 and NF-κB1, mRNA and protein expression of NF-κB1 were detected by qRT-PCR and Western blotting. Data showed that miR-16 upregulation dramatically reduced the protein expression of NF-κB1. Meanwhile, we observed that NF-κB1 expression was increased by downregulating miR-16 (Fig.2c,d). Thus, miR-16 inhibited NF-κB1 expression in human glioma.

Bottom Line: MicroRNA-16 decreased glioma malignancy by downregulating NF-κB1 and MMP9, and led to suppressed invasiveness of human glioma cell lines SHG44, U87, and U373.Our results also indicated that upregulation of miR-16 promoted apoptosis by suppressing BCL2 expression.Finally, the upregulation of miR-16 in a nude mice model of human glioma resulted in significant suppression of glioma growth and invasiveness.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.

Show MeSH
Related in: MedlinePlus