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. 2020 Jun 5;20(2):1989–1998. doi: 10.3892/ol.2020.11699

Figure 2.

Figure 2.

STAT3 inhibition suppresses human diffuse intrinsic pontine glioma cell viability. SF8628 cells were treated with vehicle control (DMSO) or AG490. SF8628 cells were transfected shCtrl or shSTAT3. (A) mRNA STAT3 expression was determined via reverse transcription-semi-quantitative PCR. β-actin mRNA was used as the loading control. (B) Cell viability data of AG490-treated cells. Cells were treated with various concentrations of AG490. Cell viability was analyzed using a CCK-8 assay, and absorbance was measured at 420 nm. *P<0.05 vs. DMSO-treated cells using one-way ANOVA. Data are presented as the mean ± SD. (C and D) CCK-8 assay of control cells and STAT3-inhibited cells. Cell viability was analyzed using a CCK-8 assay, and absorbance was measured at 420 nm. *P<0.05 vs. DMSO-treated cells or shCtrl-transfected cells at 48 h using a two-tailed unpaired Student's t-test. Data are presented as the mean ± SD. (E) Western blot analysis of pSTAT3, total STAT3 and cyclin D1. Protein samples were extracted from SF8628 control cells and STAT3-inhibited cells; β-actin was used as the loading control. Exposure time was 3 min for pSTAT3, 1 min for STAT3, 30 sec for cyclin D1 and 15 sec for β-actin. STAT3, signal transducer and activator of transcription 3; pSTAT3, phosphorylated STAT3; shCtrl, control short hairpin RNA; shSTAT3, STAT3 short hairpin RNA; CCK-8, Cell Counting Kit-8.