Cell Signaling Technology Inc tgf β

SETD2 inactivation induces a <t>TGF‐β‐independent</t> EMT program. (A) Cell morphology of WT, TGF‐β‐treated WT, and SETD2 KO RPTEC. Magnification 10×. Scale bar, 400 μm. (B) RT‐qPCR results for expression of epithelial and mesenchymal genes in WT, TGF‐β‐treated WT, and SETD2 KO clones. Data from three replicates are represented as mean ± SEM. P ‐value is calculated for epithelial and mesenchymal genes individually using one‐way ANOVA. **** P < 0.0001; *** P < 0.001; * P < 0.05; ns, P ≥ 0.05. (C) Western blot showing expression of EMT markers in the indicated cell lines. (D) Western blot for <t>total</t> <t>SMAD2</t> and phospho (Ser465/467) SMAD2, and TGF‐β levels in WT, SETD2 KO, SETD2 KO rescue, and TGF‐β‐treated/untreated WT RPTEC cells. Images in C and D are representative of three independent experiments. (E) Top panel: volcano plot of differentially expressed genes between TGF‐β‐treated WT and untreated control. Bottom panel: differentially expressed genes between SETD2 KO and WT RPTEC (genes shown are common between the two independent KO1/2 clones). Average value of log2‐fold change for each gene is used as the expression value. Green: downregulated genes (log2‐fold change < −1 and P < 0.05). Red: upregulated genes (log2‐fold change > 1 and P < 0.05). EMT genes are labeled. RNA‐seq was run in duplicate. (F) Heatmaps of all differentially expressed genes between SETD2‐deficient or TGF‐β treatment and RPTEC WT (top), and a subset of key genes linked to EMT, IFNγ, and secreted factors shown in the lower panel. ‘a/b’ denote replicates. (G) Venn diagram of differentially expressed genes between parental RPTEC, SETD2 KO RPTEC, and TGF‐β‐treated WT RPTEC. (H) Heatmap comparing enrichment of select GSEA hallmark pathways for differentially expressed genes between RPTEC WT/SETD2 KO (yellow), RPTEC TGF‐β‐treated vs control (blue), and TCGA primary SETD2 mutant vs WT tumors (green). P ‐values are derived from the GSEA algorithm (Broad Institute); * P < 0.05. H3, histone H3; MW, molecular weight.

Tgf β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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triosephosphate isomerase antibody 3711 dylight 488 (Novus Biologicals)

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SETD2 inactivation induces a TGF‐β‐independent EMT program. (A) Cell morphology of WT, TGF‐β‐treated WT, and SETD2 KO RPTEC. Magnification 10×. Scale bar, 400 μm. (B) RT‐qPCR results for expression of epithelial and mesenchymal genes in WT, TGF‐β‐treated WT, and SETD2 KO clones. Data from three replicates are represented as mean ± SEM. P ‐value is calculated for epithelial and mesenchymal genes individually using one‐way ANOVA. **** P < 0.0001; *** P < 0.001; * P < 0.05; ns, P ≥ 0.05. (C) Western blot showing expression of EMT markers in the indicated cell lines. (D) Western blot for total SMAD2 and phospho (Ser465/467) SMAD2, and TGF‐β levels in WT, SETD2 KO, SETD2 KO rescue, and TGF‐β‐treated/untreated WT RPTEC cells. Images in C and D are representative of three independent experiments. (E) Top panel: volcano plot of differentially expressed genes between TGF‐β‐treated WT and untreated control. Bottom panel: differentially expressed genes between SETD2 KO and WT RPTEC (genes shown are common between the two independent KO1/2 clones). Average value of log2‐fold change for each gene is used as the expression value. Green: downregulated genes (log2‐fold change < −1 and P < 0.05). Red: upregulated genes (log2‐fold change > 1 and P < 0.05). EMT genes are labeled. RNA‐seq was run in duplicate. (F) Heatmaps of all differentially expressed genes between SETD2‐deficient or TGF‐β treatment and RPTEC WT (top), and a subset of key genes linked to EMT, IFNγ, and secreted factors shown in the lower panel. ‘a/b’ denote replicates. (G) Venn diagram of differentially expressed genes between parental RPTEC, SETD2 KO RPTEC, and TGF‐β‐treated WT RPTEC. (H) Heatmap comparing enrichment of select GSEA hallmark pathways for differentially expressed genes between RPTEC WT/SETD2 KO (yellow), RPTEC TGF‐β‐treated vs control (blue), and TCGA primary SETD2 mutant vs WT tumors (green). P ‐values are derived from the GSEA algorithm (Broad Institute); * P < 0.05. H3, histone H3; MW, molecular weight.

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: SETD2 inactivation induces a TGF‐β‐independent EMT program. (A) Cell morphology of WT, TGF‐β‐treated WT, and SETD2 KO RPTEC. Magnification 10×. Scale bar, 400 μm. (B) RT‐qPCR results for expression of epithelial and mesenchymal genes in WT, TGF‐β‐treated WT, and SETD2 KO clones. Data from three replicates are represented as mean ± SEM. P ‐value is calculated for epithelial and mesenchymal genes individually using one‐way ANOVA. **** P < 0.0001; *** P < 0.001; * P < 0.05; ns, P ≥ 0.05. (C) Western blot showing expression of EMT markers in the indicated cell lines. (D) Western blot for total SMAD2 and phospho (Ser465/467) SMAD2, and TGF‐β levels in WT, SETD2 KO, SETD2 KO rescue, and TGF‐β‐treated/untreated WT RPTEC cells. Images in C and D are representative of three independent experiments. (E) Top panel: volcano plot of differentially expressed genes between TGF‐β‐treated WT and untreated control. Bottom panel: differentially expressed genes between SETD2 KO and WT RPTEC (genes shown are common between the two independent KO1/2 clones). Average value of log2‐fold change for each gene is used as the expression value. Green: downregulated genes (log2‐fold change < −1 and P < 0.05). Red: upregulated genes (log2‐fold change > 1 and P < 0.05). EMT genes are labeled. RNA‐seq was run in duplicate. (F) Heatmaps of all differentially expressed genes between SETD2‐deficient or TGF‐β treatment and RPTEC WT (top), and a subset of key genes linked to EMT, IFNγ, and secreted factors shown in the lower panel. ‘a/b’ denote replicates. (G) Venn diagram of differentially expressed genes between parental RPTEC, SETD2 KO RPTEC, and TGF‐β‐treated WT RPTEC. (H) Heatmap comparing enrichment of select GSEA hallmark pathways for differentially expressed genes between RPTEC WT/SETD2 KO (yellow), RPTEC TGF‐β‐treated vs control (blue), and TCGA primary SETD2 mutant vs WT tumors (green). P ‐values are derived from the GSEA algorithm (Broad Institute); * P < 0.05. H3, histone H3; MW, molecular weight.

Article Snippet: Primary antibodies used are CDH1 (Cell Signaling Technology, Beverly, MA, USA; #3195S), MUC1 (Abcam, Boston, MA, USA; #ab109185), SNAI2 (Cell Signaling Technology; #9585S), MMP2 (Proteintech, Rosemont, IL, USA; #10373‐2‐AP), CD44 (GeneTex, Irvine, CA, USA; GTX102111), CD34 (Proteintech; 60180), vimentin (Santa Cruz Biotechnology; B0719), total SMAD2 (Cell Signaling Technology; #3103S), phosphorylated SMAD2 (Cell Signaling Technology; #3108S), TGF‐β (Cell Signaling Technology; #3711S), H3K36me1 (Abcam; #ab9048), H3K36me2 (Cell Signaling Technology; #2901S), H3K36me3 (Active Motif; #61101), histone H3 (Abcam; #ab1791), SOX2 (R&D Systems; #AF2018‐SP), OCT2 (Thermo Fisher; #39‐5400), PRRX1 (Novus Biologicals, St. Charles, MO, USA; #NBP1‐06067), anti‐FLAG (Sigma‐Aldrich; #F1804), GAPDH (Cell Signaling Technology; #2118S), and lamin B1 (Proteintech; #12987‐1‐AP).

Techniques: Quantitative RT-PCR, Expressing, Clone Assay, Western Blot, Control, Labeling, RNA Sequencing, Mutagenesis, Derivative Assay, Molecular Weight

SETD2 loss drives EMT and stemness phenotypes. (A) Wound healing assay assessing migratory phenotype for 72 h TGF‐β treatment of RPTEC WT (left panel) vs untreated control and SETD2 KO vs WT/rescue (right panel). P ‐value for comparing wound closure among WT, SETD2 KO, and SETD2 KO rescue RPTEC, each performed in duplicate, is calculated using one‐way ANOVA. Data are represented as mean ± SEM. Magnification 4×. Scale bar, 1000 μm. (B) Transwell assay testing invasiveness of TGF‐β‐treated WT cells. Magnification 2.5×. Scale bar, 1200 μm. (C) Transwell assay testing invasiveness of WT, SETD2 KO, and SETD2 KO rescue RPTEC. For B and C images of crystal violet‐stained cells that invaded through the membrane are shown beside the graphs. Two‐way ANOVA is used for statistical testing; samples are run in duplicate. Data are represented as mean ± SEM. Magnification 2.5×. Scale bar, 1200 μm. (D) 3D spheroid formation assay evaluating stemness in SETD2 KO cells. Data are represented as mean ± SEM. Image of spheroids in ultra‐low attachment plates are shown at the right. P ‐value is calculated using one‐way ANOVA. Magnification 4×. Scale bar, 1000 μm. **** P < 0.0001; *** P < 0.001; ** P < 0.01; * P < 0.05; ns, P ≥ 0.05.

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: SETD2 loss drives EMT and stemness phenotypes. (A) Wound healing assay assessing migratory phenotype for 72 h TGF‐β treatment of RPTEC WT (left panel) vs untreated control and SETD2 KO vs WT/rescue (right panel). P ‐value for comparing wound closure among WT, SETD2 KO, and SETD2 KO rescue RPTEC, each performed in duplicate, is calculated using one‐way ANOVA. Data are represented as mean ± SEM. Magnification 4×. Scale bar, 1000 μm. (B) Transwell assay testing invasiveness of TGF‐β‐treated WT cells. Magnification 2.5×. Scale bar, 1200 μm. (C) Transwell assay testing invasiveness of WT, SETD2 KO, and SETD2 KO rescue RPTEC. For B and C images of crystal violet‐stained cells that invaded through the membrane are shown beside the graphs. Two‐way ANOVA is used for statistical testing; samples are run in duplicate. Data are represented as mean ± SEM. Magnification 2.5×. Scale bar, 1200 μm. (D) 3D spheroid formation assay evaluating stemness in SETD2 KO cells. Data are represented as mean ± SEM. Image of spheroids in ultra‐low attachment plates are shown at the right. P ‐value is calculated using one‐way ANOVA. Magnification 4×. Scale bar, 1000 μm. **** P < 0.0001; *** P < 0.001; ** P < 0.01; * P < 0.05; ns, P ≥ 0.05.

Techniques: Wound Healing Assay, Control, Transwell Assay, Staining, Membrane, Tube Formation Assay

SETD2 rescue partially restores global transcriptional patterns and reverses EMT and stemness transcriptional signatures. (A) Principal component analysis of all genes in untreated RPTEC WT, SETD2 KO, SETD2 KO rescue, and TGF‐β‐treated WT RPTEC derived from RNA‐seq (all lines are run in duplicate). (B) A scatterplot of RPTEC KO vs WT against SETD2 rescue vs KO showing reversal of genes differentially expressed with SETD2 loss with ectopic re‐expression of SETD2. A subset of key EMT genes is labeled in red. (C) A heatmap of hallmark pathways from GSEA altered in SETD2 KO and reversed with ectopic re‐expression. (D) A subset of reversed pathways from (C) demonstrating reversal of EMT and IFNγ pathways with reintroduction of SETD2. Two genes of interest are indicated (PRRX1 and OAS2), and the differential expression and gene rank in their respective comparisons are shown, along with the pathway normalized enrichment score (NES) and adjusted P ‐value ( P adj).

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: SETD2 rescue partially restores global transcriptional patterns and reverses EMT and stemness transcriptional signatures. (A) Principal component analysis of all genes in untreated RPTEC WT, SETD2 KO, SETD2 KO rescue, and TGF‐β‐treated WT RPTEC derived from RNA‐seq (all lines are run in duplicate). (B) A scatterplot of RPTEC KO vs WT against SETD2 rescue vs KO showing reversal of genes differentially expressed with SETD2 loss with ectopic re‐expression of SETD2. A subset of key EMT genes is labeled in red. (C) A heatmap of hallmark pathways from GSEA altered in SETD2 KO and reversed with ectopic re‐expression. (D) A subset of reversed pathways from (C) demonstrating reversal of EMT and IFNγ pathways with reintroduction of SETD2. Two genes of interest are indicated (PRRX1 and OAS2), and the differential expression and gene rank in their respective comparisons are shown, along with the pathway normalized enrichment score (NES) and adjusted P ‐value ( P adj).

Techniques: Derivative Assay, RNA Sequencing, Expressing, Labeling, Quantitative Proteomics

SOX2, OCT2, and PRRX1 are downstream effectors of the SETD2‐regulated EMT program. (A) Expression of SOX2, OCT2, and PRRX1 in TGF‐β‐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 4× magnification, scale bar: 1000 μm for (B) and (D) and at 2.5× magnification, scale bar: 1200 μm 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.

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: SOX2, OCT2, and PRRX1 are downstream effectors of the SETD2‐regulated EMT program. (A) Expression of SOX2, OCT2, and PRRX1 in TGF‐β‐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 4× magnification, scale bar: 1000 μm for (B) and (D) and at 2.5× magnification, scale bar: 1200 μm 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.

Techniques: Expressing, Quantitative RT-PCR, Migration, Wound Healing Assay, Transwell Assay, Tube Formation Assay, Control, Plasmid Preparation

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