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Fig. 2 | Molecular Cancer

Fig. 2

From: Knockdown of SOX2OT inhibits the malignant biological behaviors of glioblastoma stem cells via up-regulating the expression of miR-194-5p and miR-122

Fig. 2

MiR-194-5p and miR-122 exerted tumor-suppressive functions in GSCs. a The expression of miR-194-5p in normal brain tissues (NBTs) and glioma tissues of different grades. Data are presented as the mean Â± SD (NBTs (n = 5), Grade I (n = 5), Grade II (n = 5), Grade III (n = 8), Grade IV (n = 8)). ** P < 0.01 vs. NBTs group; ## P < 0.01 vs. Grade I group; △△ P < 0.01 vs. Grade II group; ΨΨ P < 0.01 vs. Grade III group. The expression of miR-194-5p in human astrocytes (HA), glioblastoma cell lines (U87 and U251) and glioblastoma stem cells (GSC-U87, GSC-U251). Data are presented as the mean Â± SD (n = 5,each group). ** P < 0.01 vs. HA group; ## P < 0.01 vs. U87 group; △△ P < 0.01 vs. U251 group. b The expression of miR-194-5p after SOX2OT knockdown in GSC-U87 and GSC-U251 cells. ** P < 0.01 vs. sh-NC group. c The predicted miR-194-5p binding site in the SOX2OT sequence (SOX2OT-Wt) and the designed mutant sequence of miR-194-5p binding site (SOX2OT-Mut) are indicated. Relative luciferase activity was conducted after cells were transfected with SOX2OT-Wt or SOX2OT-Mut. Data were presented as the mean Â± SD (n = 5, each group). ** P < 0.01 vs. SOX2OT-Wt + Agomir-194-5p-NC. d CCK-8 assay was used to measure the effect of miR-194-5p on the proliferation of GSC-U87 and GSC-U251 cells. e The apoptotic percentages of GSC-U87 and GSC-U251 cells were detected after miR-194-5p over-expression or inhibition. f Transwell assays was used to measure the effect of miR-194-5p on the migration and invasion of GSC-U87 and GSC-U251 cells. Scale bars represent 40 Î¼m. Data are presented as the mean Â± SD (n = 5, each group).** P < 0.01 vs. Agomir-194-5p-NC group; ## P < 0.01 vs. Antagomir-194-5p-NC group. g The expression of miR-122 in normal brain tissues(NBTs) and glioma tissues of different grades. Data are presented as the mean Â± SD (NBTs (n = 5), Grade I (n = 5), Grade II(n = 5), Grade III (n = 8), Grade IV (n = 8)). ** P < 0.01 vs. NBTs group; ## P < 0.01 vs. Grade I group; △△ P < 0.01 vs. Grade II group; ΨΨ P < 0.01 vs. Grade III group. The expression of miR-122 in HA cells, glioblastoma cell lines(U87 and U251) and glioblastoma stem cells (GSC-U87, GSC-U251). Data are presented as the mean Â± SD (n = 5,each group). ** P < 0.01 vs. HA group; ## P < 0.01 vs. U87 group; △△ P < 0.01 vs. U251 group. h The expression of miR-122 with SOX2OT knockdown in GSC-U87 and GSC-U251 cells. ** P < 0.01 vs. sh-NC group. i The predicted miR-122 binding sites in the SOX2OT sequence (SOX2OT-Wt) and the designed mutant sequence of miR-122 binding site (SOX2OT-Mut) are indicated. Relative luciferase activity was conducted after cells were transfected with SOX2OT-Wt or SOX2OT-Mut. Data were presented as the mean Â± SD (n = 5, each group). ** P < 0.01 vs. SOX2OT-Wt + Agomir-122-NC. j CCK-8 assay was used to measure the effect of miR-122 on the proliferation of GSC-U87 and GSC-U251 cells. k The apoptotic percentages of GSC-U87 and GSC-U251 cells were detected after miR-122 over-expression or inhibition. l Transwell assays were used to measure the effect of miR-122 on the migration and invasion of GSC-U87 and GSC-U251 cells. Scale bars represent 40 Î¼m. Data are presented as the mean Â± SD (n = 5, each group). ** P < 0.01 vs. Agomir-122-NC group; ## P < 0.01 vs. Antagomir-122-NC group

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