Journal: Disease Models & Mechanisms

Article Title: ETV1 is a key regulator of enteroendocrine PYY production

doi: 10.1242/dmm.052610

Figure Lengend Snippet: Etv1 expression is most strongly correlated with expression of Gcg , Pyy and Cck in vivo . (A) Workflow for analysis of enteroendocrine cells (EECs) from the single-cell RNA-sequencing (scRNA-seq) dataset published by . PCA, principal component analysis; UMAP, Uniform Manifold Approximation and Projection. (B) Expression of Etv1 across different cell type clusters (original cell type annotation). TA, transit amplifying. (C) UMAP plot following unsupervised clustering of EECs from mouse small intestine. Clusters are annotated based on expression of known marker genes with a temporal expression pattern during EEC differentiation. EC, enterochromaffin cell. (D) Violin plots showing expression of selected genes involved in EEC differentiation across cell type clusters of EECs from mouse small intestine. (E) UMAP plot showing expression levels of Etv1 in EECs from mouse small intestine. (F) Correlation between Etv1 expression and expression of different enteroendocrine (EE) hormones. R-value=Pearson correlation coefficient. (G-I) UMAP plots showing expression of Gcg (G), Pyy (H) and Cck (I) in EECs from mouse small intestine.

Article Snippet: The Etv1 gene insert in pLX_TRC311_ETV1 ( Addgene plasmid #74981 ) was cloned into SP170 (PB-TRE-DEST-IRES-BSD) (a kind gift from Steve Pollard's laboratory, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK) using gateway cloning.

Techniques: Expressing, In Vivo, RNA Sequencing, Marker

Journal: Disease Models & Mechanisms

Article Title: ETV1 is a key regulator of enteroendocrine PYY production

doi: 10.1242/dmm.052610

Figure Lengend Snippet: EEC differentiation and Etv1 expression in organoid cultures resemble in vivo observations. (A) Expression of Etv1 across different cell type clusters (cell type annotation from ). (B) UMAP plot following unsupervised clustering of EECs from organoid cultures. Clusters are annotated based on expression of known marker genes with a temporal expression pattern during EEC differentiation. (C) Violin plots showing expression of selected transcription factors involved in EEC differentiation across cell type clusters of EECs in organoids. (D) UMAP plot showing expression levels of Etv1 in EECs from organoids. (E) Correlation between Etv1 expression and expression of different EE hormones in organoid cultures. R-value=Pearson correlation coefficient.

Article Snippet: The Etv1 gene insert in pLX_TRC311_ETV1 ( Addgene plasmid #74981 ) was cloned into SP170 (PB-TRE-DEST-IRES-BSD) (a kind gift from Steve Pollard's laboratory, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK) using gateway cloning.

Techniques: Expressing, In Vivo, Marker

Journal: Disease Models & Mechanisms

Article Title: ETV1 is a key regulator of enteroendocrine PYY production

doi: 10.1242/dmm.052610

Figure Lengend Snippet: Etv1 mutant cultures have reduced Pyy expression. (A) Strategy for generation of Etv1 mutant organoid lines. Ngn3, Neurog3 . Created in BioRender by Jensen Team (2025). https://BioRender.com/eqtfeop . This figure was sublicensed under CC-BY 4.0 terms. (B) Amplified and sequenced Etv1 cDNA aligned to the Etv1 gene using the BLAT alignment tool. Screenshot downloaded from http://genome.ucsc.edu . (C) ETV1 protein (transcript variant 1). One dot corresponds to one amino acid (AA). Skipping of exon 8 changes AA 186-187 from phenylalanine (F) and arginine (R) to serine (S) and alanine (A) and introduces a premature stop codon after AA187, resulting in a protein that lacks the DNA binding domain (orange dots). (D-G) Expression of Etv1 (D), Gcg (E), Cck (F) and Pyy (G) in control and Etv1 mutant organoid cultures. The Etv1 reverse primer is located within exon 8. Expression is normalised to expression of Gapdh. Error bars indicate s.d. ( n =3). Significance was evaluated with an unpaired two-tailed t -test. CTRL, control. (H,I) Percentage of Neurog3-RFP + (H) and Gcg-Venus + (I) cells in control (two lines) and Etv1 mutant (three lines) organoid cultures assessed by flow cytometry. Error bars indicate s.d. Significance was evaluated with an unpaired two-tailed t -test. (J,K) Expression of Etv1 (J) and Pyy (K) in control and Etv1 mutant organoid cultures treated for 3 days with or without 10 µg DAPT and/or 20 ng/ml BMP-4. Significance was evaluated with an unpaired two-tailed t -test. ns, not significant; * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001.

Article Snippet: The Etv1 gene insert in pLX_TRC311_ETV1 ( Addgene plasmid #74981 ) was cloned into SP170 (PB-TRE-DEST-IRES-BSD) (a kind gift from Steve Pollard's laboratory, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK) using gateway cloning.

Techniques: Mutagenesis, Expressing, Amplification, Variant Assay, Binding Assay, Control, Two Tailed Test, Flow Cytometry

Journal: Disease Models & Mechanisms

Article Title: ETV1 is a key regulator of enteroendocrine PYY production

doi: 10.1242/dmm.052610

Figure Lengend Snippet: Etv1 mutant organoids show no overall changes in cell type composition but lack EECs with high Pyy expression. (A) UMAP plot of cells from both control (two lines) and Etv1 mutant (three lines) organoids following scRNA-seq (1158 cells in total). Cell types are annotated based on expression of known marker genes ( Fig. S4A ). (B) UMAP plot of cells from control (left) and Etv1 mutant (right) organoids (control, 494 cells; Etv1 mutant, 664 cells). (C) Percentage of cells found in each of the identified cell clusters in control (two lines) and Etv1 mutant (three lines) organoids. Error bars indicate s.d. Significance was evaluated with an unpaired two-tailed t -test. ns, not significant. (D) Violin plots showing expression levels of known cell type and proliferation marker genes in control (orange) and Etv1 mutant (green) organoids. (E) UMAP plot showing EECs in control (orange) and Etv1 mutant (green) organoids. (F) UMAP plot showing expression levels of Etv1 , Gcg , Cck and Pyy in EECs from control (top row) and Etv1 mutant (bottom row) organoids.

Article Snippet: The Etv1 gene insert in pLX_TRC311_ETV1 ( Addgene plasmid #74981 ) was cloned into SP170 (PB-TRE-DEST-IRES-BSD) (a kind gift from Steve Pollard's laboratory, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK) using gateway cloning.

Techniques: Mutagenesis, Expressing, Control, Marker, Two Tailed Test

Journal: Disease Models & Mechanisms

Article Title: ETV1 is a key regulator of enteroendocrine PYY production

doi: 10.1242/dmm.052610

Figure Lengend Snippet: Etv1 overexpression increases expression of Pyy and Cck , but not Gcg . (A) Strategy for generation of Etv1 -overexpressing ( Etv1 OE) organoids. SI, small intestine. Created in BioRender by Jensen Team (2025). https://BioRender.com/eqtfeop . This figure was sublicensed under CC-BY 4.0 terms. (B) Images of control and Etv1 OE organoids with and without 48 h of doxycycline treatment. Scale bars: 275 µm. Organoids were derived from a Neurog3 -RFP; Gcg -Venus mouse ( ; ). (C) Expression of Etv1 , Pyy , Gcg , Cck , Sct and Ngn3 ( Neurog3 ) in control and Etv1 OE organoid cultures with and without 48 h doxycycline treatment. Error bars indicate s.d. ( n =3). Expression is normalised to expression of 36B4 ( Rplp0 ). Significance was evaluated with a one-way ANOVA. (D) Luciferase activity in inducible Etv1 OE HEK293 cells transfected with a pGL4.23 vector containing either a wild-type (PyyProm_WT) or mutated (PyyProm_MUT) version of a 517 bp region upstream of Pyy covering two putative ETV1 binding sites ( Fig. S7A ). Luciferase activity was normalised to the activity in HEK293 cells transfected with a pGL4.23 vector without any insert. Where indicated, cells were treated for 24 h with doxycycline (1 mg/ml). Error bars indicate s.d. ( n =4). Significance was evaluated with an unpaired two-tailed t -test. ns, not significant; * P <0.05, ** P <0.01.

Article Snippet: The Etv1 gene insert in pLX_TRC311_ETV1 ( Addgene plasmid #74981 ) was cloned into SP170 (PB-TRE-DEST-IRES-BSD) (a kind gift from Steve Pollard's laboratory, Centre for Regenerative Medicine, University of Edinburgh, Edinburgh, UK) using gateway cloning.

Techniques: Over Expression, Expressing, Control, Derivative Assay, Luciferase, Activity Assay, Transfection, Plasmid Preparation, Binding Assay, Two Tailed Test

Journal: Journal of Immunology (Baltimore, Md. : 1950)

Article Title: Gene expression profiling and real-time PCR analyses identify novel potential cancer-testis antigens in multiple myeloma

doi: 10.4049/jimmunol.0803298

Figure Lengend Snippet: Known and novel CT gene expression patterns determined by real-time PCR.

Article Snippet: For each genes, a, b, c are MMC samples showing a Present call with a high Affymetrix signal (above the median); d and e are MMC samples showing a Present call with a low Affymetrix signal (under the median). table ft1 table-wrap mode="anchored" t5 caption a7 CT gene category Taqman gene assay Gene name Chromosomal Location number of positive 1 somatic tissues Positive somatic tissues Ratio MMC/Testis 2 (qPCR) Ratio MMC/NT Max 3 (qPCR) Frequency in MM patients (n=64) 4 (Affymetrix) Testis- restricted Hs00218682_m1 DDX43 chr6q12-q13 0 0.1 5.8 34% Hs00366532_m1 MAGEA3 chrXq28 0 2.9 28915.2 33% Hs00193821_m1 MAGEC1 chrXq26 0 7.0 70208.3 66% Hs00212255_m1 MAGEC2 chrXq27 0 0.5 460.7 13% Hs00205327_m1 MORC1 chr3q13 0 0.7 204.9 36% Hs00846692_s1 SSX1 chrXp11 0 15.4 153600.7 20% Hs00258708_m1 TEX14 chr17q22 0 0.3 41.1 16% Tissue- restricted Hs00265824_m1 CTAG1B chrXq28 1 Brain 9.6 78.1 13% Hs00189285_m1 CTNNA2 chr2p12-p11.1 1 Brain 1.6 1.0 27% Hs00396095_m1 LOC130576 chr2q23.2 1 Stomach 1.0 4.4 47% Hs01395126_m1 FAM133A chrXq21.32 1 Brain 0.7 5.1 53% Hs01651017_m1 ANKRD45 chr1q25.1 2 Lung, brain 0.2 0.5 16% Hs00224122_m1 ELOVL4 chr6q14 2 Brain, stomach 2.6 1.8 25% Hs00541322_m1 IGSF11 chr3q13.32 2 Brain, adrenal gland 0.3 1.8 39% Hs00186495_m1 TMEFF1 chr9q31 2 Brain, lung 2.0 0.9 20% Hs00249367_m1 TMEFF2 chr2q32.3 2 Brain, stomach 1.6 0.3 11% Differentially expressedUbiquitously expressed Hs00332514_m1 FLJ23577 chr5p13.2 3 Pancreas, liver, lung 0.2 0.4 47% Hs01096927_m1 NOL4 chr18q12 3 Brain, pancreas 0.2 0.1 59% Hs00417254_m1 PTPN20A chr10q11.22 3 Heart, adrenal gland, kidney 0.2 1.1 25% Hs00292465_m1 ARX chrXp22.1- 3 4 Brain, pancreas, lung, skeletal muscle 19.6 16.5 17% Hs00418637_g1 LOC150763 chr2q11.2 4 Pancreas, bone marrow, lung, adrenal gland 1.1 3.6 27% Hs00382529_m1 MGC3040 chr3q21 5 Lung, brain, bone marrow, adrenal gland, skeletal muscle 1.0 0.8 31% Hs00162127_m1 SPAG4 chr20q11.21 6 Pancreas, stomach, liver, intestine, bone marrow, adrenal gland 8.4 2.3 100% Ubiquitously expressed Hs00231877_m1 ETV1 chr7p21.3 7 Lung, adrenal gland, liver, stomach, pancreas, heart, brain 0.2 0.1 45% Hs00214398_m1 FLJ20130 chrXq22.3 7 Adrenal gland, liver, pancreas, kidney, intestine, bone marrow, lung 1.5 2.4 41% Hs00177193_m1 PTPRG chr3p21-p14 9 Lung, brain, stomach, liver, pancreas, kidney, intestine, heart, adrenal gland 2.9 0.9 80% Open in a separate window Gene names written in Bold are known CT genes.

Techniques: Gene Expression, Gene Assay

Journal: eLife

Article Title: The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression

doi: 10.7554/eLife.77072

Figure Lengend Snippet: ( A ) CIC transcriptionally represses ETV1/4/5. ( B ) The 19q13.2 genomic locus demonstrating the physical location of ERF and CIC . ( C ) 15 PCa studies (cBioPortal) demonstrating the co-occurrence of ERF and CIC homozygous and heterozygous deletions. The co-occurrence of ERF and CIC alterations is highly significant (p<0.001 co-occurrence, Fisher exact test). ( D ) ERF-CIC co-deleted PCa stratified by Gleason score and tumor stage. ( E ) Frequency of ERF and CIC alterations in primary PCa (top) and metastatic castrate resistant prostate cancer (mCRPC; bottom), demonstrating enrichment in mCRPC. ( F ) Onco-print of known genetic drivers (ERG, ETV1, ETV4, SPOP, and FOXA1) of PCa aligned with CIC and ERF (cBioPortal). CIC-ERF co-deleted prostate tumors (red box) do not frequently co-occur with other known oncogenic events. ( G ) Survival analysis performed using 15 PCa datasets from cBioPortal. Disease-free survival (DFS) and progression-free survival (PFS) in patients harboring the ERF-CIC co-deletion (red) vs. no ERF-CIC co-deletion (blue). p=value, log-rank. Figure 1—source data 1. Prostate cancer studies identified in cBioPortal demonstrating the total number of patients, number of patients with shallow or deep deletions in Capicua (CIC)-ETS2 repressor factor (ERF), and the frequency of CIC-ERF alterations in each cohort. Studies that analyzed predominantly primary prostate cancers (green) and metastatic castrate resistant prostate cancer (mCRPC; yellow) are highlighted.

Article Snippet: Human CIC (Cat#. Hs00943425_g1), ERF (Cat#. Hs01100070_g1), ETV1 (Cat#. Hs00951951_m1), ETV4 (Cat#. Hs00383361_g1), ETV5 (Cat#. Hs00927557_m1), and endogenous controls GAPDH (Cat#. Hs02758991_g1) were amplified with Taqman gene expression assay (Applied Biosystems).

Techniques:

Journal: eLife

Article Title: The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression

doi: 10.7554/eLife.77072

Figure Lengend Snippet: ( A ) Percentage of CIC and ERF peaks located in defined genomic regions. ( B ) Schematic algorithm to identify shared CIC and ERF target genes in prostate cells (top). Functional Clustering Analysis of the 91 shared CIC and ERF target genes using DAVID (bottom table). ( C ) ETV1 mRNA expression in prostate epithelial cells (PNT2) ( CIC-ERF -replete) cells with ERF knockdown (KD), CIC knockout (KO), or ERF KD + CIC KO (n=3). ( D ) Schematic of CIC and ERF DNA-binding motifs in the ETV1 promoter. ( E ) Chromatin immunoprecipitation (ChIP)-PCR from PNT2 cells showing CIC occupancy on the ETV1 promoter. ( F–G ) ChIP-PCR with ERF occupancy on the ETV1 promoter. ( H ) ETV1 mRNA expression in DU-145 (ERF-deficient) cells with ERF rescue, CIC KO, or ERF rescue + CIC KO (n=3). ETV1 mRNA expression in PC-3 cells with ( I ) ERF KD (n=3) and ( J ) ERF overexpression (OE) (n=3). p Values were calculated using Student’s t test. *p<0.05, **p<0.01, and ****p<0.0001. Error bars represent SD. Performed in triplicate. ( K ) ETV1 luciferase promoter assay in 293T cells comparing Empty vector (EV) with ERF OE (n=6). Student’s t test, *p<0.05. Error bars represent SD. ( L ) Single sample gene set enrichment analysis (ssGSEA) alignments comparing gene expression patterns in PNT2 cells with ERF KD and CIC KO. IC = information coefficient. Figure 4—source data 1. Full-length PCR gel images of ETV1 after Capicua (CIC) pull down in prostate epithelial cells (PNT2). Cropped images and description shown in . Figure 4—source data 2. Full-length PCR gel images of ETV1 after ETS2 repressor factor (ERF) pull down in prostate epithelial cells (PNT2). Cropped images and description shown in . Figure 4—source data 3. Full-length PCR gel images of ETV1 after ETS2 repressor factor (ERF) pull down in DU-145 cells. Cropped images and description shown in .

Article Snippet: Human CIC (Cat#. Hs00943425_g1), ERF (Cat#. Hs01100070_g1), ETV1 (Cat#. Hs00951951_m1), ETV4 (Cat#. Hs00383361_g1), ETV5 (Cat#. Hs00927557_m1), and endogenous controls GAPDH (Cat#. Hs02758991_g1) were amplified with Taqman gene expression assay (Applied Biosystems).

Techniques: Functional Assay, Expressing, Knockdown, Knock-Out, Binding Assay, Chromatin Immunoprecipitation, Over Expression, Luciferase, Promoter Assay, Plasmid Preparation, Gene Expression

Journal: eLife

Article Title: The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression

doi: 10.7554/eLife.77072

Figure Lengend Snippet: ( A–C ) Relative ETV1 , ETV4 , and ETV5 mRNA expression in prostate epithelial cells (PNT2) parental and PNT2 CIC knockout (KO) cells (n=3). ( D–F ) Relative ETV1 , ETV4 , and ETV5 mRNA expression in PNT2 parental and PNT2 ERF knockdown (KD) + CIC KO cells (n=3). ( G ) Relative ERF , ( H ) ETV1 , ( I ) ETV4 , and ( J ) ETV5 mRNA expression in parental PNT2 and PNT2 ERF KD cells (n=3). ( K ) Co-immunoprecipitation using GFP-tagged ERF (pulldown) and immunoblotting for ERF and CIC. ( L ) Co-immunoprecipitation using Myc-tagged CIC (pulldown) and immunoblotting for ERF and CIC. ( M ) ETV1 chromatin immunoprecipitation (ChIP)-PCR fold enrichment of CIC compared to IgG control in PNT2 cells (n=3). ( N ) ETV1 ChIP-PCR fold enrichment of ERF compared to IgG control in PNT2 cells (n=3). ( O ) Gene Desert quantitative PCR (Active Motif Negative control) comparing CIC and ERF to IgG control. ( P ) Gene Desert quantitative PCR (Active Motif Negative control) comparing CIC, ERF, and IgG to input control. Relative ( Q ) ERF , ( R ) ETV1 , ( S ) ETV4 , and ( T ) ETV5 mRNA expression in parental DU-145 and DU-145 ERF cells (n=3). p Values for all figures = *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001. Error bars represent SD. Figure 4—figure supplement 1—source data 1. Co-immunoprecipitation using GFP-tagged ETS2 repressor factor (ERF) and immunoblotting for Capicua (CIC; bottom panel) and ETS2 repressor factor (ERF; top panel) with associated raw images. Figure 4—figure supplement 1—source data 2. Co-immunoprecipitation using myc-tagged Capicua (CIC) and immunoblotting for ETS2 repressor factor (ERF; top panel) and CIC (bottom panel) with associated raw images.

Article Snippet: Human CIC (Cat#. Hs00943425_g1), ERF (Cat#. Hs01100070_g1), ETV1 (Cat#. Hs00951951_m1), ETV4 (Cat#. Hs00383361_g1), ETV5 (Cat#. Hs00927557_m1), and endogenous controls GAPDH (Cat#. Hs02758991_g1) were amplified with Taqman gene expression assay (Applied Biosystems).

Techniques: Expressing, Knock-Out, Knockdown, Immunoprecipitation, Western Blot, Chromatin Immunoprecipitation, Control, Real-time Polymerase Chain Reaction, Negative Control

Journal: eLife

Article Title: The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression

doi: 10.7554/eLife.77072

Figure Lengend Snippet: ( A–C ) Relative ETV1 , ATAD2, and ID2 mRNA expression in LNCaP cells with or without BMS32048 (ETV1 inhibitor) treatment (n=3). ( D ) Relative ETV1 mRNA expression in PC-3 cells, ( E ) DU-145 +sgCIC1 and ( F ) DU-145 +sgCIC2 with or without si ETV1 (n=3). p values for all figures = **p<0.01, ***p<0.001, ****p<0.0001.

Article Snippet: Human CIC (Cat#. Hs00943425_g1), ERF (Cat#. Hs01100070_g1), ETV1 (Cat#. Hs00951951_m1), ETV4 (Cat#. Hs00383361_g1), ETV5 (Cat#. Hs00927557_m1), and endogenous controls GAPDH (Cat#. Hs02758991_g1) were amplified with Taqman gene expression assay (Applied Biosystems).

Techniques: Expressing

Journal: eLife

Article Title: The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression

doi: 10.7554/eLife.77072

Figure Lengend Snippet: ( A ) DU-145 cells were transfected with either siScramble (siSCM) or si CIC . After 48 hr, BRD32048 (ETV1 inhibitor) was added to both the transfected groups at the defined concentrations (0 μM, 25 μM, 50 μM). After 24 hr of BRD32048 treatment, cells were replated for crystal violet assay (0.4%) and images were taken and analyzed after 5 days (n=3). siCIC was compared to siSCRM conditions in each respective drug concentration. ( B ) Crystal violet viability assay (n=3). si ETV1 groups were compared to siSCRM control groups +/- CIC expression (sgCtrl, sgCIC1, or sgCIC2). ( C ) DU-145 cells were transfected with either siScramble (siSCM) or si CIC . After 48 hr, BRD32048 was added to the transfected groups at defined concentrations (0 μM or 50 μM). Transwell invasion assays (n=3) were performed 24 hr after the addition of BRD32048. siCIC was compared to siSCRM in the 0 μM and 50 μM concentration groups. ( D ) Transwell invasion assays (n=3) comparing si ETV1 to siSCRM control +/-CIC expression (sgCtrl, sgCIC1, or sgCIC2). p value = *p<0.05, **p<0.01 for all figures. Error bars represent SD.

Article Snippet: Human CIC (Cat#. Hs00943425_g1), ERF (Cat#. Hs01100070_g1), ETV1 (Cat#. Hs00951951_m1), ETV4 (Cat#. Hs00383361_g1), ETV5 (Cat#. Hs00927557_m1), and endogenous controls GAPDH (Cat#. Hs02758991_g1) were amplified with Taqman gene expression assay (Applied Biosystems).

Techniques: Transfection, Crystal Violet Assay, Concentration Assay, Viability Assay, Control, Expressing

Journal: eLife

Article Title: The CIC-ERF co-deletion underlies fusion-independent activation of ETS family member, ETV1, to drive prostate cancer progression

doi: 10.7554/eLife.77072

Figure Lengend Snippet:

Article Snippet: Human CIC (Cat#. Hs00943425_g1), ERF (Cat#. Hs01100070_g1), ETV1 (Cat#. Hs00951951_m1), ETV4 (Cat#. Hs00383361_g1), ETV5 (Cat#. Hs00927557_m1), and endogenous controls GAPDH (Cat#. Hs02758991_g1) were amplified with Taqman gene expression assay (Applied Biosystems).

Techniques: Transfection, Construct, shRNA, Plasmid Preparation, Sequencing

Journal: eLife

Article Title: Extracellular signal-regulated kinase mediates chromatin rewiring and lineage transformation in lung cancer

doi: 10.7554/elife.66524

Figure Lengend Snippet: Figure 6. The roles of ETS family transcription factors in the regulation of neuroendocrine differentiation in small cell lung cancer cell lines. (a) Upregulated genes by KRASG12V overexpression for 1 day and 7 days in comparison with a GFP overexpression control in H2107 and H82 cells. The numbers of genes upregulated (>1.5 fold) are indicated. ETV1, ETV4, and ETV5 are shown in red. (b) Heat map of the PEA3 family ETS transcription factors (ETV1, ETV4, and ETV5) and neuroendocrine transcription factors (ASCL1, NEUROD1, INSM1, and POU3F2 [BRN2]) in small cell lung cancer and Figure 6 continued on next page

Article Snippet: Human ETV1 (Addgene, Cambridge, MA, USA; plasmid #82209) and ETV5 (Horizon Discovery, Cambridge, UK; clone 100008315) were transferred to pInducer20 using Gateway LR Clonase II enzyme mix (Thermo Fisher Scientific).

Techniques: Over Expression, Comparison, Control