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Image Search Results
Journal: Molecular oncology
Article Title: SETD2 loss in renal epithelial cells drives epithelial-to-mesenchymal transition in a TGF-β-independent manner.
doi: 10.1002/1878-0261.13487
Figure Lengend Snippet: Fig. 7. SOX2, OCT2, and PRRX1 are downstream effectors of the SETD2-regulated EMT program. (A) Expression of SOX2, OCT2, and PRRX1 in TGF-b-treated WT (72 h), SETD2 KO, and SETD2 rescue tested by RT-qPCR (run in triplicate). (B) Migration capacity by wound healing assay, (C) invasiveness by transwell assay, and (D) stemness by 3D spheroid formation assay in RPTEC WT GFP (control vector), SETD2 KO1 and KO2, and SOX2/OCT2/PRRX1-transduced WT RPTEC lines. Images are taken at 49 magnification, scale bar: 1000 lm for (B) and (D) and at 2.59 magnification, scale bar: 1200 lm for (C). Data are represented as mean SEM for triplicate reactions for B–D. P-value is calculated by one-way ANOVA in (A), (B), and (D). Two-way ANOVA is used for statistical test for (C). ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05; ns, P ≥0.05. (E) Model of the SETD2 loss-driven EMT program through cell intrinsic (transcriptional) and cell extrinsic (paracrine) mechanisms.
Article Snippet: See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense #ab1791),
Techniques: Expressing, Quantitative RT-PCR, Migration, Wound Healing Assay, Transwell Assay, Tube Formation Assay, Control, Plasmid Preparation