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. 2019 May 16;10(6):381. doi: 10.1038/s41419-019-1614-1

Fig. 4.

Fig. 4

Knockdown of PGC1α partly rescued the effect of knockdown of miR-23b in OS. a Knockdown efficacy of PGC1α in miR-23b-3p knockdown MNNG-HOS and MG63 cells were determined by western blotting. b, c PGC1α knockdown partly reversed the inhibitory effects of miR-23b-3p knockdown on the colony-formation properties of OS (MNNG-HOS and MG63) cells, values are means ± SD, **p < 0.01, ***p < 0.001. d Silencing of PGC1α partly reversed the inhibitory effects of miR-23b-3p knockdown on the CCK-8 assay of MNNG-HOS and MG63 cells, values are means ± SD, *p < 0.05, **p < 0.01. e PGC1α knockdown partly reversed the inhibitory effects of miR-23b-3p silencing on the proliferation properties of MNNG-HOS cells. Excised tumors from different groups are shown (n = 4). Scale bars = 1 cm. f PGC1α knockdown partly rescued the inhibitory effects of miR-23b-3p knockdown on the growth rate in MNNG-HOS cells in vivo. Tumor volumes were measured with calipers every 5 days, values are means ± SD, **p < 0.01. g, h Altered level of OCR and ECAR in OS cells (MNNG-HOS and MG63) in different groups (Control, knockdown-miR-23b-3p, knockdown-miR-23b-3p, and knockdown- PGC1α). Values are means ± SD. i, j. ATP level and lactate production were determined in different groups (Control, knockdown-miR-23b-3p, knockdown-miR-23b-3p, and knockdown-PGC1α). Values are means ± SD, *p < 0.05, **p < 0.01, ***p < 0.001