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Fig. 3 | Stem Cell Research & Therapy

Fig. 3

From: Sin3a drives mesenchymal-to-epithelial transition through cooperating with Tet1 in somatic cell reprogramming

Fig. 3

RNA-seq reveals Sin3a deficiency impedes MET process. A Volcano plot of differentially expressed genes (red, upregulated genes; blue, downregulated genes) after Sin3a knockdown. B The top 10 enriched GO terms for the differentially expressed genes (GO-Down, downregulated genes, left; GO-Up, upregulated genes, right) in the Sin3a knockdown group are shown. C Heatmap for the MET-related genes in the shSin3a-1 group compared to the control. D Representative images of the cell morphology of the control and Sin3a knockdown groups at Day 5 and Day 8 of MEF reprogramming. Black arrows indicate the representative cell–cell contact morphology. E, F qRT-PCR analysis of the expression changes of mesenchymal markers (E) and epithelial markers (F) at Day 5 and Day 8 of MEF reprogramming after Sin3a knockdown. G GO term analysis for the significantly downregulated genes in the Sin3a knockdown group is shown. H Western blotting analysis of SIN3A, E-cadherin, and β-catenin expression at Day 5 and Day 8 of MEF reprogramming. GAPDH was used as loading control. I Flow cytometry detection of the percentage of E-cadherin and β-catenin positive cells in the control and Sin3a knockdown groups at Day 8 of MEF reprogramming. Significance was estimated by student’s unpaired t test. Data in E, F, and I were representative of three independent experiments. *P < 0.05, **P < 0.01, and ***P < 0.001 versus the control group at Day 5. #P < 0.05, ##P < 0.01, and ###P < 0.001 versus the control group at Day 8. Error bars represent SD

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