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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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miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.
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fig06: miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.

Mentions: Finally, to test the effects of miR-16 on glioma growth in vivo, we used a mouse model of human glioma. As shown in our experiments, all tumors from U87 cells transfected with plasmid-connected pre-miR-16 were efficiently suppressed compared with the negative control (Fig.5c,d). The intracranial tumors were removed and sectioned. Hematoxylin–eosin staining showed that miR-16 reduced glioma growth and invasion in the encephalic nude mouse model (Fig.5a). Immunofluorescence showed that miR-16 reduced glioma invasion and MMP9 expression in the nude encephalic mouse model (Fig.5b). Sections were stained for Ki-67, MMP9, and NF-κB1. Immunohistochemistry showed that tumors with U87 cells transfected with miR-16 reduced Ki-67 (Fig.6a), MMP9 (Fig.6b), and NF-κB1 stainings (Fig.6c), compared with negative control oligonucleotide. Thus, the data indicated that miR-16 upregulation led to the inhibition of glioma cell proliferation and invasion in tumor xenografts, and that the upregulation of miR-16 reduced glioma growth in the mouse model in vivo.


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)

miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317940&req=5

fig06: miR-16 reduced Ki-67 (a), MMP9 (b), and nuclear factor-κB1 (NF-κB1) (c) expression in an in vivo mouse model using U87 glioma cells. miR-16, microRNA-16.
Mentions: Finally, to test the effects of miR-16 on glioma growth in vivo, we used a mouse model of human glioma. As shown in our experiments, all tumors from U87 cells transfected with plasmid-connected pre-miR-16 were efficiently suppressed compared with the negative control (Fig.5c,d). The intracranial tumors were removed and sectioned. Hematoxylin–eosin staining showed that miR-16 reduced glioma growth and invasion in the encephalic nude mouse model (Fig.5a). Immunofluorescence showed that miR-16 reduced glioma invasion and MMP9 expression in the nude encephalic mouse model (Fig.5b). Sections were stained for Ki-67, MMP9, and NF-κB1. Immunohistochemistry showed that tumors with U87 cells transfected with miR-16 reduced Ki-67 (Fig.6a), MMP9 (Fig.6b), and NF-κB1 stainings (Fig.6c), compared with negative control oligonucleotide. Thus, the data indicated that miR-16 upregulation led to the inhibition of glioma cell proliferation and invasion in tumor xenografts, and that the upregulation of miR-16 reduced glioma growth in the mouse model in vivo.

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