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Addgene inc smad2 overexpressed vector
Smad2 Overexpressed Vector, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/smad2 overexpressed vector/product/Addgene inc
Average 93 stars, based on 5 article reviews

smad2 overexpressed vector - by Bioz Stars, 2026-05

93/100 stars

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A PCA of AR and IgG RIME data in AR positive cell lines. B Barplot representing the enriched nuclear proteins (LFQ difference > 1 & p-value < 0.05) per cell line assigned to the displayed subsets. Shared = found in all AR positive cell lines and not in PC3. Sig in all = found across all cell lines. Sig in PC3 = proteins significant in PC3 and another cell line. AR dep unique = Shared between LNCaP, LAPC4 and no other. AR indep unique = shared between CWR-R1, 22Rv1, LNCaP-abl and 42D and no other. AR-V7 unique = proteins shared in cell lines that express the alternative AR splive variant AR-V7 (CWR-R1, 22Rv1, Supplementary Figure 3A ) C Over representation analysis of the AR core proteins against the CORUM protein complex database D Volcano plot displaying the TRIM33 RIME data with the AR core proteins highlighted in orange. Triangles depict proteins enriched in IgG with fold changes out of the axis limits. E Euler Diagram of the AR core, LNCaP AR and TRIM33 RIME nuclear enriched proteins.

Journal: bioRxiv

Article Title: TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

doi: 10.1101/2025.02.14.638236

Figure Lengend Snippet: A PCA of AR and IgG RIME data in AR positive cell lines. B Barplot representing the enriched nuclear proteins (LFQ difference > 1 & p-value < 0.05) per cell line assigned to the displayed subsets. Shared = found in all AR positive cell lines and not in PC3. Sig in all = found across all cell lines. Sig in PC3 = proteins significant in PC3 and another cell line. AR dep unique = Shared between LNCaP, LAPC4 and no other. AR indep unique = shared between CWR-R1, 22Rv1, LNCaP-abl and 42D and no other. AR-V7 unique = proteins shared in cell lines that express the alternative AR splive variant AR-V7 (CWR-R1, 22Rv1, Supplementary Figure 3A ) C Over representation analysis of the AR core proteins against the CORUM protein complex database D Volcano plot displaying the TRIM33 RIME data with the AR core proteins highlighted in orange. Triangles depict proteins enriched in IgG with fold changes out of the axis limits. E Euler Diagram of the AR core, LNCaP AR and TRIM33 RIME nuclear enriched proteins.

Article Snippet: Guides targeting TRIM33 (T33-3: 5’-ACAGAGTCTGTTGGAGCATC-3, T33-4: 5’-ACTATGGCAAATGCAAACCG-3, T33-5: 5’-CTCCTCCTCCACCAGCACCG-3) or non-targeting control (NT: 5’-AACTACAAGTAAAAGTATCG-3) were cloned into lentiCRISPRv2 plasmids ( Addgene: #52961).

Techniques: Variant Assay

A Feature distribution of peaks identified in the given ChIP-seq experiment. For AR, ChIP-seq data from GSE94682 was used B Over representation analysis of peak associated genes. Shown are only genesets that have a p.adjust < 0.05. C Tornado plot for the TRIM33 and AR shared and unique peaks at 4h stimulation. Data represents the average of QC passing replicates. D Tornado plot for the TRIM33 sites with dynamic behavior. Data represents the average of QC passing replicates. E Average signal intensity plots for the regions shown in D. Lighter colors represent the DMSO control whereas darker colors represent stimulated conditions with R1881. F GIGGLE results for the TRIM33 sites gained after 4h of R1881 treatment

Journal: bioRxiv

Article Title: TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

doi: 10.1101/2025.02.14.638236

Figure Lengend Snippet: A Feature distribution of peaks identified in the given ChIP-seq experiment. For AR, ChIP-seq data from GSE94682 was used B Over representation analysis of peak associated genes. Shown are only genesets that have a p.adjust < 0.05. C Tornado plot for the TRIM33 and AR shared and unique peaks at 4h stimulation. Data represents the average of QC passing replicates. D Tornado plot for the TRIM33 sites with dynamic behavior. Data represents the average of QC passing replicates. E Average signal intensity plots for the regions shown in D. Lighter colors represent the DMSO control whereas darker colors represent stimulated conditions with R1881. F GIGGLE results for the TRIM33 sites gained after 4h of R1881 treatment

Techniques: ChIP-sequencing, Control

A Western blot for TRIM33 across the generated monoclonal knockout cell lines of the TRIM33-5 guide. B Incucyte growth curves of monoclonal TRIM33 knockout cell lines in FBS. As an error SEM is shown. C Euler diagram for all DEGs in the represented cell lines between DMSO and 6h R1881 stimulation. D Heatmap for DEGs in the non-targeting control across all sequenced LNCaP cell lines. PC represents the TRIM33 polyclonal knockout parental cell line. E Volcano plot of gene expression levels between TRIM33 monoclonal knockout C2 and the non-targeting control at 6h stimulation with R1881. Genes in green are higher expressed in non-targeting cells than knockout cells. F GSEA of the data in E. Shown are only genesets that have a p.adjust < 0.05. G Scatterplot of the Cistrome-Go analysis. Used are the TRIM33 peaks at 4h stimulation and the RNA foldchange showed in E. Triangles depict AR response genes as defined by differential expression status in non-targeting control with and without AR stimulation. Cut-off for regulatory potential was set to 0.3. H Scatterplot comparing TRIM33 knockout (C2) to non-targeting foldchanges on RNA (x-axis) and protein (y-axis) levels. Genes or proteins just found in one dataset were set to 0 in the other. The dashed line represents the diagonal with a slope of 1. Cut-offs for classification were a foldchange > 1 for RNA and > 0.5 for proteomic data. I GSEA of proteomic data of all tested TRIM33 knockouts in R1881 treated conditions compared to the non-targeting. NTvs represents the comparison of non-targeting cells with and without stimulation.

Journal: bioRxiv

Article Title: TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

doi: 10.1101/2025.02.14.638236

Figure Lengend Snippet: A Western blot for TRIM33 across the generated monoclonal knockout cell lines of the TRIM33-5 guide. B Incucyte growth curves of monoclonal TRIM33 knockout cell lines in FBS. As an error SEM is shown. C Euler diagram for all DEGs in the represented cell lines between DMSO and 6h R1881 stimulation. D Heatmap for DEGs in the non-targeting control across all sequenced LNCaP cell lines. PC represents the TRIM33 polyclonal knockout parental cell line. E Volcano plot of gene expression levels between TRIM33 monoclonal knockout C2 and the non-targeting control at 6h stimulation with R1881. Genes in green are higher expressed in non-targeting cells than knockout cells. F GSEA of the data in E. Shown are only genesets that have a p.adjust < 0.05. G Scatterplot of the Cistrome-Go analysis. Used are the TRIM33 peaks at 4h stimulation and the RNA foldchange showed in E. Triangles depict AR response genes as defined by differential expression status in non-targeting control with and without AR stimulation. Cut-off for regulatory potential was set to 0.3. H Scatterplot comparing TRIM33 knockout (C2) to non-targeting foldchanges on RNA (x-axis) and protein (y-axis) levels. Genes or proteins just found in one dataset were set to 0 in the other. The dashed line represents the diagonal with a slope of 1. Cut-offs for classification were a foldchange > 1 for RNA and > 0.5 for proteomic data. I GSEA of proteomic data of all tested TRIM33 knockouts in R1881 treated conditions compared to the non-targeting. NTvs represents the comparison of non-targeting cells with and without stimulation.

Techniques: Western Blot, Generated, Knock-Out, Control, Gene Expression, Quantitative Proteomics, Comparison

A PCA plots for grouped and individual analysis of the TRIM33 C2 knockout ChIP-seq data. B Average signal intensity profiles of AR (top) and H3K18ac (bottom) across the tested cell lines on the TRIM33 R1881 treatment gained and lost regions of . TRIM33 C2 knockout cells are in green and non-targeting in blue. C Heatmap of H2Bub signal across gene bodies of differentially expressed genes from as well as the unresponsive genes. D Average signal intensity plots for the regions depicted in C. E Distribution of the sum of the H2Bub signals across the scaled gene body from the regions in C. Significance levels of Wilcoxon ranked sum test: * < 0.01, ** < 0.001

Journal: bioRxiv

Article Title: TRIM33 loss reduces Androgen Receptor transcriptional output and H2BK120 ubiquitination

doi: 10.1101/2025.02.14.638236

Figure Lengend Snippet: A PCA plots for grouped and individual analysis of the TRIM33 C2 knockout ChIP-seq data. B Average signal intensity profiles of AR (top) and H3K18ac (bottom) across the tested cell lines on the TRIM33 R1881 treatment gained and lost regions of . TRIM33 C2 knockout cells are in green and non-targeting in blue. C Heatmap of H2Bub signal across gene bodies of differentially expressed genes from as well as the unresponsive genes. D Average signal intensity plots for the regions depicted in C. E Distribution of the sum of the H2Bub signals across the scaled gene body from the regions in C. Significance levels of Wilcoxon ranked sum test: * < 0.01, ** < 0.001

Techniques: Knock-Out, ChIP-sequencing

TRIM33 is phosphorylated by RSK at S1119. A , HEK293 cells were transfected with HA-tagged TRIM33, serum-starved overnight, and stimulated for 10 or 20 min with fetal bovine serum (FBS; 10%), EGF (25 ng/ml), insulin (100 nM), or PMA (50 ng/ml). Immunoprecipitated TRIM33 was then assayed for phosphorylation with a phospho-motif antibody that recognizes the RxxS∗/T∗ consensus motif. B , same as in ( A ), except cells were pretreated with PD184352 (10 μM) or BI-D1870 (10 μM) for 30 min prior to PMA stimulation. C , as in ( A ), except cells were transfected with HA-tagged TRIM33 WT or the S1119A unphosphorylable mutant. D , detection of phospho-RxxS∗/T∗ in TRIM33-WT and -S1119A in WT and RSK-DKO HeLa cells. Cells transfected with the HA-tagged TRIM33 constructs were stimulated for 30 min with PMA prior to HA immunoprecipitation. PMA, phorbol 12-myristate 13-acetate; RSK, ribosomal S6 kinase.

Journal: The Journal of Biological Chemistry

Article Title: Identification of RSK substrates using an analog-sensitive kinase approach

doi: 10.1016/j.jbc.2024.105739

Figure Lengend Snippet: TRIM33 is phosphorylated by RSK at S1119. A , HEK293 cells were transfected with HA-tagged TRIM33, serum-starved overnight, and stimulated for 10 or 20 min with fetal bovine serum (FBS; 10%), EGF (25 ng/ml), insulin (100 nM), or PMA (50 ng/ml). Immunoprecipitated TRIM33 was then assayed for phosphorylation with a phospho-motif antibody that recognizes the RxxS∗/T∗ consensus motif. B , same as in ( A ), except cells were pretreated with PD184352 (10 μM) or BI-D1870 (10 μM) for 30 min prior to PMA stimulation. C , as in ( A ), except cells were transfected with HA-tagged TRIM33 WT or the S1119A unphosphorylable mutant. D , detection of phospho-RxxS∗/T∗ in TRIM33-WT and -S1119A in WT and RSK-DKO HeLa cells. Cells transfected with the HA-tagged TRIM33 constructs were stimulated for 30 min with PMA prior to HA immunoprecipitation. PMA, phorbol 12-myristate 13-acetate; RSK, ribosomal S6 kinase.

Article Snippet: The original plasmid encoding human TRIM33 (pCS2-FLAG-hEcto/Tif1g) was obtained from Dr Stefano Piccolo through Addgene (#20902).

Techniques: Transfection, Immunoprecipitation, Phospho-proteomics, Mutagenesis, Construct

Fig. 1 | Deletion of Trim33 abates replicative stress. a Immunoblotting analysis of p19/Nras Trim33-WT and Trim33-KO cell lines; n = 3. b Analysis of the RNA-seq data for two Trim33-KO cell lines; n = 3. Venn diagram shows the number of commonly deregulated genes (p adj <0.01, any log2FC) for the two knockout cell lines com- pared to Trim33-WT cells. Top three enriched KEGG pathways are shown (analyzed by Enrichr70). c DNA ﬁber assays in Trim33-WT and Trim33-KO cells expressing Myc or a Ctrl vector; n = 2. 100 ﬁbers were measured per sample; scale bar = 1 μm. Sig- niﬁcance was determined using Kruskal–Wallis test and Dunn’s multiple compar- isons. d Immunoblotting analysis in Trim33-WT and Trim33-KO cells expressing Myc or Ctrl vector; n = 3. e DNA ﬁber assays in Trim33-WT and Trim33-KO cells, unchallenged (Ctrl) or released from a 4-h hydroxyurea (HU) treatment (HU-rel); n = 3. 100 ﬁbers were measured per sample; signiﬁcance was determined as in c). Scale bar = 1 μm. f EdU incorporation analysis in Ctrl and HU-treated Trim33-WT

Journal: Nature communications

Article Title: Trim33 masks a non-transcriptional function of E2f4 in replication fork progression.

doi: 10.1038/s41467-023-40847-0

Figure Lengend Snippet: Fig. 1 | Deletion of Trim33 abates replicative stress. a Immunoblotting analysis of p19/Nras Trim33-WT and Trim33-KO cell lines; n = 3. b Analysis of the RNA-seq data for two Trim33-KO cell lines; n = 3. Venn diagram shows the number of commonly deregulated genes (p adj <0.01, any log2FC) for the two knockout cell lines com- pared to Trim33-WT cells. Top three enriched KEGG pathways are shown (analyzed by Enrichr70). c DNA ﬁber assays in Trim33-WT and Trim33-KO cells expressing Myc or a Ctrl vector; n = 2. 100 ﬁbers were measured per sample; scale bar = 1 μm. Sig- niﬁcance was determined using Kruskal–Wallis test and Dunn’s multiple compar- isons. d Immunoblotting analysis in Trim33-WT and Trim33-KO cells expressing Myc or Ctrl vector; n = 3. e DNA ﬁber assays in Trim33-WT and Trim33-KO cells, unchallenged (Ctrl) or released from a 4-h hydroxyurea (HU) treatment (HU-rel); n = 3. 100 ﬁbers were measured per sample; signiﬁcance was determined as in c). Scale bar = 1 μm. f EdU incorporation analysis in Ctrl and HU-treated Trim33-WT

Article Snippet: Trim33 expression vectors were a gift of Stefano Piccolo (Addgene plasmids # 20902 and 20903).

Techniques: Western Blot, RNA Sequencing, Knock-Out, Expressing, Plasmid Preparation

Fig. 3 | Deletion of Trim33 promotes E2f4 interactions with chromatin and with the Recql helicase. a Genome browser tracks of E2f4 ChIP-seq in p19/Nras Trim33- WT and Trim33-KO cells; n = 2. b Quantiﬁcation of ChIP-seq tag coverage at E2f4 peaks in p19/Nras Trim33-WT and Trim33-KO cells. c Relationship between changes (log2FC) in E2f4 binding (normalized E2f4 ChIP-seq tags) and mRNA expression (log2FC) of the encoded gene for p19/Nras Trim33-KO vs Trim33-WT cells. Each dot is a bin of 5 genes sorted by the change in mRNA levels. Trendlines are derived from linear regression analysis. d LC-MS/MS analysis of E2f4 interactome in p19/Nras Trim33-WT and Trim33-KO cells. Known interaction partners are highlighted in blue. e PLA analysis of Recql-E2f4 association in p19/Nras Trim33-WT and Trim33- KO cells stably expressing HA-tagged E2f4 or vector Ctrl; from left, n = 49,49,50,50

Journal: Nature communications

Article Title: Trim33 masks a non-transcriptional function of E2f4 in replication fork progression.

doi: 10.1038/s41467-023-40847-0

Figure Lengend Snippet: Fig. 3 | Deletion of Trim33 promotes E2f4 interactions with chromatin and with the Recql helicase. a Genome browser tracks of E2f4 ChIP-seq in p19/Nras Trim33- WT and Trim33-KO cells; n = 2. b Quantiﬁcation of ChIP-seq tag coverage at E2f4 peaks in p19/Nras Trim33-WT and Trim33-KO cells. c Relationship between changes (log2FC) in E2f4 binding (normalized E2f4 ChIP-seq tags) and mRNA expression (log2FC) of the encoded gene for p19/Nras Trim33-KO vs Trim33-WT cells. Each dot is a bin of 5 genes sorted by the change in mRNA levels. Trendlines are derived from linear regression analysis. d LC-MS/MS analysis of E2f4 interactome in p19/Nras Trim33-WT and Trim33-KO cells. Known interaction partners are highlighted in blue. e PLA analysis of Recql-E2f4 association in p19/Nras Trim33-WT and Trim33- KO cells stably expressing HA-tagged E2f4 or vector Ctrl; from left, n = 49,49,50,50

Article Snippet: Trim33 expression vectors were a gift of Stefano Piccolo (Addgene plasmids # 20902 and 20903).

Techniques: ChIP-sequencing, Binding Assay, Expressing, Derivative Assay, Liquid Chromatography with Mass Spectroscopy, Stable Transfection, Plasmid Preparation

a) Volcano plot showing the enrichment of proteins immunoprecipitated from DOX-treated over untreated ESC DUXBL-LG by using two independent ESC lines from a representative DUXBL IP-MS experiment. Enriched proteins in DOX-treated cells are highlighted in red. b) Western blot analysis of the indicated proteins performed with FLAG immunoprecipitates obtained from untreated or DOX-treated ESC DUXBL-LG . c) Immunofluorescence analysis of endogenous DUXBL and TRIM24 in untreated or DOX-treated LTR-RFP reporter WT or TRIM24 KO ESC DUX . DAPI was used to visualize nuclei. Scale bars, 20 μm. Dashed regions are zoomed-in in the insets. Three independent experiments using two WT and TRIM24 KO ESC DUX clones were performed but one representative experiment is shown. d) Immunofluorescence analysis of endogenous TRIM33 and TRIM24 in untreated or DOX-treated LTR-RFP reporter ESC DUX . DAPI was used to visualize nuclei. Scale bars, 20 μm. Dashed regions are zoomed-in in the insets. Three independent experiments using two ESC DUX clones were performed but one representative experiment is shown. e) High-throughput imaging quantification of the number of DUXBL foci per cell (upper panel), the total intensity of DUXBL foci per cell (middle panel) and the total area of DUXBL foci per cell (lower panel) in untreated or DOX-treated LTR-RFP reporter WT or TRIM24 KO ESC DUX . Center lines indicate mean values. n=2000; Percentages above the threshold (dotted line) are indicated. Relevant p values are shown from one-tailed unpaired t -tests. Three independent experiments using at least two WT or TRIM24 KO ESC DUX clones were performed but one representative experiment is shown. f) Immunofluorescence analysis of endogenous DUXBL and TRIM24 at different timepoints in untreated or DOX-treated WT ESC DUX . Time since the addition of DOX is indicated. DAPI was used to visualize nuclei. Scale bar, 20 μm.

Journal: bioRxiv

Article Title: The homeobox transcription factor DUXBL controls exit from totipotency

doi: 10.1101/2022.09.19.508541

Figure Lengend Snippet: a) Volcano plot showing the enrichment of proteins immunoprecipitated from DOX-treated over untreated ESC DUXBL-LG by using two independent ESC lines from a representative DUXBL IP-MS experiment. Enriched proteins in DOX-treated cells are highlighted in red. b) Western blot analysis of the indicated proteins performed with FLAG immunoprecipitates obtained from untreated or DOX-treated ESC DUXBL-LG . c) Immunofluorescence analysis of endogenous DUXBL and TRIM24 in untreated or DOX-treated LTR-RFP reporter WT or TRIM24 KO ESC DUX . DAPI was used to visualize nuclei. Scale bars, 20 μm. Dashed regions are zoomed-in in the insets. Three independent experiments using two WT and TRIM24 KO ESC DUX clones were performed but one representative experiment is shown. d) Immunofluorescence analysis of endogenous TRIM33 and TRIM24 in untreated or DOX-treated LTR-RFP reporter ESC DUX . DAPI was used to visualize nuclei. Scale bars, 20 μm. Dashed regions are zoomed-in in the insets. Three independent experiments using two ESC DUX clones were performed but one representative experiment is shown. e) High-throughput imaging quantification of the number of DUXBL foci per cell (upper panel), the total intensity of DUXBL foci per cell (middle panel) and the total area of DUXBL foci per cell (lower panel) in untreated or DOX-treated LTR-RFP reporter WT or TRIM24 KO ESC DUX . Center lines indicate mean values. n=2000; Percentages above the threshold (dotted line) are indicated. Relevant p values are shown from one-tailed unpaired t -tests. Three independent experiments using at least two WT or TRIM24 KO ESC DUX clones were performed but one representative experiment is shown. f) Immunofluorescence analysis of endogenous DUXBL and TRIM24 at different timepoints in untreated or DOX-treated WT ESC DUX . Time since the addition of DOX is indicated. DAPI was used to visualize nuclei. Scale bar, 20 μm.

Article Snippet: To generate DUXBL, TRIM24 and TRIM33 knockout ESC lines, we independently infected a suspension of ESC with lentiviral supernatants, generated by using LentiCRISPRv2 (gift from Feng Zhang, 52961, Addgene), encoding sgRNAs designed to target the corresponding protein (Supplementary Table 8 for sgRNA sequences).

Techniques: Immunoprecipitation, Protein-Protein interactions, Western Blot, Immunofluorescence, Clone Assay, High Throughput Screening Assay, Imaging, One-tailed Test

The expression of TRIM33 in pan-cancer, and association between TRIM33 expression and the survival of patients with GC. (A) TRIM33 expression in 31 tumors from TCGA database. Red bars represent tumor samples, blue bars represent normal tissue samples. (B) OS, FPS, and PPS curves in patients with GC. (C) Survival curves of different pTNM stages in patients with GC. (D) Survival curves of different pT stages in patients with GC. * P < .05, ** P < .01, *** P < .001 versus normal tissue samples.

Journal: Technology in Cancer Research & Treatment

Article Title: Downregulation of TRIM33 Promotes Survival and Epithelial–Mesenchymal Transition in Gastric Cancer

doi: 10.1177/15330338221114505

Figure Lengend Snippet: The expression of TRIM33 in pan-cancer, and association between TRIM33 expression and the survival of patients with GC. (A) TRIM33 expression in 31 tumors from TCGA database. Red bars represent tumor samples, blue bars represent normal tissue samples. (B) OS, FPS, and PPS curves in patients with GC. (C) Survival curves of different pTNM stages in patients with GC. (D) Survival curves of different pT stages in patients with GC. * P < .05, ** P < .01, *** P < .001 versus normal tissue samples.

Article Snippet: The GC cell lines (BGC-823, MGC-803) were purchased from Shanghai Zhong Qiao Xin Zhou Biotechnology Co., Ltd. Human gastric epithelial cells (GES) were purchased from Shanghai Huiying Biological Technology Co., Ltd, and SGC-7901 cells were a gift from Tangshan Yanyi Biotechnology Co., Ltd Roswell Park Memorial Institute (RPMI) medium and fetal bovine serum (FBS) were purchased from HyClone, and F12 Complete Medium from Zhong Qiao Xin Zhou Biotech. siRNA plasmids targeting TRIM33 were synthesized by Life Technologies, and Lipofectamine 2000 was purchased from Invitrogen.

Techniques: Expressing

Knockdown of TRIM33 promoted the proliferation of BGC-823 and SGC-7901 cells. (A&B) Western blot analysis of TRIM33 expression in GES, BGC-823, MGC-803, and SGC-7901 cell lines. (C&D) Western blot analysis of TRIM33 protein expression in cells transfected with si-TRIM33 encoding plasmids. (E) CCK8 assays were used to measure BGC-823 and SGC-7901 cell viability in the control and si-TRIM33-transfected group; the viability of the si-TRIM33 transfection groups was enhanced. (F&G) EdU assays were used to evaluate proliferation in the control and si-TRIM33 transfection groups in BGC-823 cells; the percentage of EdU-positive cells in the si-TRIM33 group was significantly greater than in the control group. * P < .05, ** P < .01; ns, non-significant.

Journal: Technology in Cancer Research & Treatment

Article Title: Downregulation of TRIM33 Promotes Survival and Epithelial–Mesenchymal Transition in Gastric Cancer

doi: 10.1177/15330338221114505

Figure Lengend Snippet: Knockdown of TRIM33 promoted the proliferation of BGC-823 and SGC-7901 cells. (A&B) Western blot analysis of TRIM33 expression in GES, BGC-823, MGC-803, and SGC-7901 cell lines. (C&D) Western blot analysis of TRIM33 protein expression in cells transfected with si-TRIM33 encoding plasmids. (E) CCK8 assays were used to measure BGC-823 and SGC-7901 cell viability in the control and si-TRIM33-transfected group; the viability of the si-TRIM33 transfection groups was enhanced. (F&G) EdU assays were used to evaluate proliferation in the control and si-TRIM33 transfection groups in BGC-823 cells; the percentage of EdU-positive cells in the si-TRIM33 group was significantly greater than in the control group. * P < .05, ** P < .01; ns, non-significant.

Techniques: Western Blot, Expressing, Transfection

Downregulation of TRIM33 enhanced colony formation and migratory ability. (A&B) Downregulation of TRIM33 promoted colony formation in BGC-823 and SGC-7901 cells. (C&D) After 24 h, the number of cells passing through the Transwell membrane was higher in the si-TRIM33 group than in the control group (×100 magnification, corresponding to a scale of 200 μm). (E&F) After 12, 24, 48, 72, 96, 120, and 144 h, the width of the residual scratch was narrower in the si-TRIM33 group than in the control group (×100 magnification, corresponding to a scale of 200 μm). * P < .05, ** P < .01.

Journal: Technology in Cancer Research & Treatment

Article Title: Downregulation of TRIM33 Promotes Survival and Epithelial–Mesenchymal Transition in Gastric Cancer

doi: 10.1177/15330338221114505

Figure Lengend Snippet: Downregulation of TRIM33 enhanced colony formation and migratory ability. (A&B) Downregulation of TRIM33 promoted colony formation in BGC-823 and SGC-7901 cells. (C&D) After 24 h, the number of cells passing through the Transwell membrane was higher in the si-TRIM33 group than in the control group (×100 magnification, corresponding to a scale of 200 μm). (E&F) After 12, 24, 48, 72, 96, 120, and 144 h, the width of the residual scratch was narrower in the si-TRIM33 group than in the control group (×100 magnification, corresponding to a scale of 200 μm). * P < .05, ** P < .01.

Techniques:

Knockdown of TRIM33 upregulated TGF-β expression. (A) ELISA analysis of TGF-β expression in the si-TRIM33 and control groups identified that knockdown of TRIM33 upregulated TGF-β expression, suggesting activation of the TGF-β signaling pathway. (B&C) Western blot analysis of the expression of proteins in the TGF-β signaling pathway in control, si-NC, and si-TRIM33 cells. Expression of p-Smad2 (Ser465/467), Smad2, Smad3, Smad4, vimentin, and N-Cadherin was upregulated, and E-Cadherin expression was downregulated, in si-TRIM33 cells. * P < .05, ** P < .01.

Journal: Technology in Cancer Research & Treatment

Article Title: Downregulation of TRIM33 Promotes Survival and Epithelial–Mesenchymal Transition in Gastric Cancer

doi: 10.1177/15330338221114505

Figure Lengend Snippet: Knockdown of TRIM33 upregulated TGF-β expression. (A) ELISA analysis of TGF-β expression in the si-TRIM33 and control groups identified that knockdown of TRIM33 upregulated TGF-β expression, suggesting activation of the TGF-β signaling pathway. (B&C) Western blot analysis of the expression of proteins in the TGF-β signaling pathway in control, si-NC, and si-TRIM33 cells. Expression of p-Smad2 (Ser465/467), Smad2, Smad3, Smad4, vimentin, and N-Cadherin was upregulated, and E-Cadherin expression was downregulated, in si-TRIM33 cells. * P < .05, ** P < .01.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Activation Assay, Western Blot

Knockdown of TRIM33 promoted GC growth in vivo. (A) The xenograft model of TRIM33-knockdown revealed that tumors were significantly larger in si-TRIM33 animals than in controls. (B&C) Immunohistochemical analysis identified that the protein levels of TRIM33, p-Smad2 (Ser465/467), Smad2, Smad3, Smad4, vimentin, and N-Cadherin were increased, and levels of E-Cadherin were decreased, in xenograft tumors from the si-TRIM33 group (×100 and ×400 magnification in left- and right-hand side images, corresponding to a scale of 200 and 50 μm, respectively).

Journal: Technology in Cancer Research & Treatment

Article Title: Downregulation of TRIM33 Promotes Survival and Epithelial–Mesenchymal Transition in Gastric Cancer

doi: 10.1177/15330338221114505

Figure Lengend Snippet: Knockdown of TRIM33 promoted GC growth in vivo. (A) The xenograft model of TRIM33-knockdown revealed that tumors were significantly larger in si-TRIM33 animals than in controls. (B&C) Immunohistochemical analysis identified that the protein levels of TRIM33, p-Smad2 (Ser465/467), Smad2, Smad3, Smad4, vimentin, and N-Cadherin were increased, and levels of E-Cadherin were decreased, in xenograft tumors from the si-TRIM33 group (×100 and ×400 magnification in left- and right-hand side images, corresponding to a scale of 200 and 50 μm, respectively).

Techniques: In Vivo, Immunohistochemical staining

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