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. 2020 Dec 30;45(3):1059–1071. doi: 10.3892/or.2020.7917

Figure 6.

Figure 6.

CASC15 depletion decreased the proliferation and promoted the apoptosis of ESCC cells by upregulating SIM2. (A) SIM2 expression was measured via reverse transcription-quantitative PCR in tumor and adjacent normal tissues isolated from patients with ESCC (n=45). (B) Linear correlation of CASC15 and SIM2 expression in ESCC tissues. (C) SIM2 protein expression was detected in HET-1A, Eca109 and KYSE450 cells via western blotting. (D) SIM2 protein expression was measured by western blotting at 48 h post transfection in Eca109 and KYSE450 cells transfected with si-NC or si-SIM2. Eca109 and KYSE450 cells were transfected with si-NC, si-CASC15#1+si-NC or si-CASC15#1+si-SIM2. (E) SIM2 protein abundance was examined via western blotting. (F) Cell proliferation was determined by performing an MTT assay in Eca109 and KYSE450 cells. Data analyzed via two-way ANOVA followed by Bonferroni's post-hoc test. (G and H) Apoptotic rate was detected via flow cytometry. (I) Relative caspase-3 activity was detected using the caspase-3 assay kit in Eca109 and KYSE450 cells. *P<0.05, **P<0.01 and ***P<0.001. CASC15, cancer susceptibility candidate 15; ESCC, esophageal squamous cell carcinoma; SIM2, single-minded 2; si, small interfering RNA; NC, negative control; OD, optical density.