Journal: Journal of Translational Medicine

Article Title: Exosomes loaded with the anti-cancer molecule mir-1-3p inhibit intrapulmonary colonization and growth of human esophageal squamous carcinoma cells

doi: 10.1186/s12967-024-05997-9

Figure Lengend Snippet: miR-1-3p directly targets and down-regulates E2F5 expression. The differentially expressed genes in the Exo-miR-1-3p group compared with the Exo-NC group, shown in the volcano plot ( A ), and the KEGG pathway analysis of differentially expressed genes ( B ). ( C ) Predicted target genes of miR-1-3p with TargetScan and miRWalk were cross-analyzed with significantly expression down-regulated genes. ( D ) E2F5 mRNA level after Exo-miR-1-3p incubation. ( E ) Putative binding sequence of miR-1-3p to the E2F5 mRNA 3’UTR and results of dual luciferase reporter assays. E2F5 protein expression of KYSE150 and Eca109 cells transfected with miR-1-3p mimics ( F ) or miR-1-3p inhibitor ( G ). Immunohistochemical staining ( H ) and H-scores ( I ) of E2F5 in mouse lung tissues. * P < 0.05, *** P < 0.001

Article Snippet: Antibodies information used in this study is provided below: anti-TSG101 (1:2000, 14497-1-AP, Proteintech), anti-CD81 (66866-1-Ig), anti-CD9 (60232-1-Ig), anti-E2F5 (1:2000, bs-1734R, Bioss), anti-GAPDH (1:5000, 60004-1-Ig, Proteintech), anti-p-p38 (1:1000, 4511, CST), anti-p38 (1:5000, 66234-1-lg, Proteintech), anti-p-ERK (1:1000, AP0974, ABclonal), anti-ERK (1:700, A4782, ABclonal), anti-p-Akt (1:2000, 28731-1-AP, Proteintech), anti-p-mTOR (1:500, AF3308, Affinity), HRP Goat anti-Rabbit IgG (1: 5000, AS014, ABclonal), HRP Goat anti-Mouse IgG (1: 5000, AS003, ABclonal).

Techniques: Expressing, Incubation, Binding Assay, Sequencing, Luciferase, Transfection, Immunohistochemical staining, Staining

Journal: Journal of Translational Medicine

Article Title: Exosomes loaded with the anti-cancer molecule mir-1-3p inhibit intrapulmonary colonization and growth of human esophageal squamous carcinoma cells

doi: 10.1186/s12967-024-05997-9

Figure Lengend Snippet: miR-1-3p inhibits proliferation and migration of ESCC cells in vitro by down-regulating E2F5. The miR-1-3p levels ( A ), E2F5 mRNA levels ( B ), and E2F5 protein levels in KYSE150 and Eca109 cells in vitro co-transfected with miR-1-3p mimics and E2F5 expression plasmids. The proliferation ( D ) and migration ( E and F ) of transfected cells. ns, no significance; * P < 0.05, *** P < 0.001

Article Snippet: Antibodies information used in this study is provided below: anti-TSG101 (1:2000, 14497-1-AP, Proteintech), anti-CD81 (66866-1-Ig), anti-CD9 (60232-1-Ig), anti-E2F5 (1:2000, bs-1734R, Bioss), anti-GAPDH (1:5000, 60004-1-Ig, Proteintech), anti-p-p38 (1:1000, 4511, CST), anti-p38 (1:5000, 66234-1-lg, Proteintech), anti-p-ERK (1:1000, AP0974, ABclonal), anti-ERK (1:700, A4782, ABclonal), anti-p-Akt (1:2000, 28731-1-AP, Proteintech), anti-p-mTOR (1:500, AF3308, Affinity), HRP Goat anti-Rabbit IgG (1: 5000, AS014, ABclonal), HRP Goat anti-Mouse IgG (1: 5000, AS003, ABclonal).

Techniques: Migration, In Vitro, Transfection, Expressing

Journal: Journal of Translational Medicine

Article Title: Exosomes loaded with the anti-cancer molecule mir-1-3p inhibit intrapulmonary colonization and growth of human esophageal squamous carcinoma cells

doi: 10.1186/s12967-024-05997-9

Figure Lengend Snippet: miR-1-3p inhibits invasion of ESCC cells in vitro by down-regulating E2F5, which may involve the MAPK/ERK signaling pathway. ( A and B ) The invasion of KYSE150 and Eca109 cells in vitro co-transfected with miR-1-3p mimics and E2F5 expression plasmids. ( C ) The protein levels of p-p38, p38, p-ERK, ERK in transfected cells, detected with western blot. ns, no significance; *** P < 0.001

Article Snippet: Antibodies information used in this study is provided below: anti-TSG101 (1:2000, 14497-1-AP, Proteintech), anti-CD81 (66866-1-Ig), anti-CD9 (60232-1-Ig), anti-E2F5 (1:2000, bs-1734R, Bioss), anti-GAPDH (1:5000, 60004-1-Ig, Proteintech), anti-p-p38 (1:1000, 4511, CST), anti-p38 (1:5000, 66234-1-lg, Proteintech), anti-p-ERK (1:1000, AP0974, ABclonal), anti-ERK (1:700, A4782, ABclonal), anti-p-Akt (1:2000, 28731-1-AP, Proteintech), anti-p-mTOR (1:500, AF3308, Affinity), HRP Goat anti-Rabbit IgG (1: 5000, AS014, ABclonal), HRP Goat anti-Mouse IgG (1: 5000, AS003, ABclonal).

Techniques: In Vitro, Transfection, Expressing, Western Blot

Journal: Nucleic Acids Research

Article Title: The p21CIP1-CDK4-DREAM axis is a master regulator of genotoxic stress-induced cellular senescence

doi: 10.1093/nar/gkae426

Figure Lengend Snippet: MCF7 cells were exposed to 1 μM B[a]P ( A, C ) or 5 Gy IR ( B, D ). Expression of E2F1, E2F4, E2F5, CCNA1, CCNA2, CCNB1, CCNB2, CCND1 and CCND2 was analysed by qPCR (A, B). ACTB and GAPDH were used as internal loading control, differences between treatment and control were statistically analysed using Student's t test (non labelled = non significant, * P < 0.1 ** P < 0.01, *** P < 0.001). Expression of E2F4, pRB, RB, pp130 and p130 was analysed by immunodetection (C, D). β-Actin or HSP90 were used as internal loading control, quantification of band intensities from two blots is shown.

Article Snippet: For gene silencing, predesigned siRNAs specific for p16 INK4A (sc-37622, Santa Cruz Biotechnology), p21 CIP1 (sc-29427, Santa Cruz Biotechnology), E2F4 (sc-29300, Santa Cruz Biotechnology) and E2F5 (sc-35250, Santa Cruz Biotechnology) were used; control human non-silencing siRNA (Silencer Select Predesigned siRNA Negative Control #1 siRNA; Ambion) was used as negative control.

Techniques: Expressing, Control, Immunodetection

Journal: Nucleic Acids Research

Article Title: The p21CIP1-CDK4-DREAM axis is a master regulator of genotoxic stress-induced cellular senescence

doi: 10.1093/nar/gkae426

Figure Lengend Snippet: ( A ) Expression of E2F4 and E2F5 was detected 48 and 72 h after siRNA-mediated knockdown by immunodetection; β-Actin was used as internal loading control; quantification of band intensities indicates knock-down efficiency. ( B, C ) MCF7 cells were treated with E2F4-, E2F5- or non-specific siRNA for 24 h and thereafter exposed to B[a]P or IR for 120 h. ( B ) Senescence was measured microscopically by β-Gal staining. ( C ) Expression of CDK1, FOXM1, MYBL2, HMGB2, CCNB1, LMNB1, PLK1, CENPF, TK1 and ASPM was measured by qPCR; ACTB and GAPDH were used as internal loading control. (B, C) Experiments were performed in triplicates, differences between treatment in absence or presence of siRNA were statistically analysed using Student's t test (non labelled = non significant, * P < 0.1 ** P < 0.01, *** P < 0.001).

Article Snippet: For gene silencing, predesigned siRNAs specific for p16 INK4A (sc-37622, Santa Cruz Biotechnology), p21 CIP1 (sc-29427, Santa Cruz Biotechnology), E2F4 (sc-29300, Santa Cruz Biotechnology) and E2F5 (sc-35250, Santa Cruz Biotechnology) were used; control human non-silencing siRNA (Silencer Select Predesigned siRNA Negative Control #1 siRNA; Ambion) was used as negative control.

Techniques: Expressing, Knockdown, Immunodetection, Control, Staining

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: Identification of E2F5 as a transcriptional target of FOXN3. (A ) Genomic distribution of FOXN3 binding sites, represented through pie charts. ( B ) Distribution of binding sites relative to transcription initiation peaks within 5 kb upstream and downstream of the transcription start site (TSS). ( C and D ) RT-qPCR ( C ) and Western blotting ( D ) analyses of E2F5 expression in THP1 cells following FOXN3 overexpression. ( E ) Scatter plot illustrating the correlation between FOXN3 and E2F5 expression levels in AML patient samples from the GSE13159 dataset, indicating a negative correlation between the two genes. ( F ) Scatter plot confirming the negative correlation between FOXN3 and E2F5 expression in AML patient samples collected from our institution. ( G ) Visualization of representative FOXN3 binding peaks in the genome browser using karyoploteR, specifically in the E2F5 promoter region. The tracks display both input and immunoprecipitation (IP) data for the Kasumi1 and THP1 cell lines. The highlighted region denotes the E2F5 promoter area, where significant binding peaks were detected in the ChIP-seq experiment. ( H ) ChIP-PCR analysis demonstrating FOXN3 binding to the E2F5 promoter. Significant enrichment of FOXN3 binding is observed at the E2F5 promoter compared to the IgG control, with the SIRT6 promoter serving as a positive control ( P = 0.001). ( I ) Results from the luciferase reporter assay illustrating the repressive effect of FOXN3 on E2F5 promoter activity. The relative luciferase activity is significantly lower in the presence of FOXN3 ( P < 0.01). Data are presented as mean ± SD of three independent experiments. Statistical significance is indicated as follows: * P < 0.05, ** P < 0.01.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques: Binding Assay, Quantitative RT-PCR, Western Blot, Expressing, Over Expression, Immunoprecipitation, ChIP-sequencing, Control, Positive Control, Luciferase, Reporter Assay, Activity Assay

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: Aberrant upregulation of E2F5 expression and its association with poor outcomes in AML. ( A ) RT-qPCR analysis showing elevated E2F5 mRNA expression in AML patients compared to healthy controls. ( B ) E2F5 mRNA levels are significantly higher in AML compared to hematopoietic stem cells (HSCs), as demonstrated using the online Bloodpool dataset. ( C ) RT-qPCR analysis revealing increased E2F5 mRNA expression in AML cell lines compared to control cell lines. ( D ) Correlation between higher E2F5 expression and shorter overall survival (OS) in AML, determined using the median value as the cutoff to distinguish between high and low E2F5 expression levels from the online GEPIA dataset. Data are presented as mean ± SD of three independent experiments. Statistical significance is indicated as follows:* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques: Expressing, Quantitative RT-PCR, Control

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: Inhibition of cell proliferation, induction of apoptosis, and cell cycle arrest following E2F5 knockdown in AML cells. ( A ) CCK-8 assay was conducted to assess the proliferation of Kasumi1 and THP1 cells following E2F5 knockdown. ( B ) Flow cytometry analysis evaluated the induction of apoptosis in Kasumi1 and THP1 cells after E2F5 knockdown. ( C ) Cell cycle analysis was performed on Kasumi1 and THP1 cells with E2F5 knockdown using flow cytometry. Data are presented as mean ± SD of three independent experiments. Statistical significance is indicated as follows: * P < 0.05, ** P < 0.01, and **** P < 0.0001.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques: Inhibition, Knockdown, CCK-8 Assay, Flow Cytometry, Cell Cycle Assay

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: Enhancement of cell proliferation and cell cycle following E2F5 overexpression in AML cells. ( A ) CCK-8 assay evaluated the proliferation of Kasumi1 and THP1 cells following E2F5 overexpression. ( B ) Cell cycle analysis was conducted on Kasumi1 and THP1 cells with E2F5 overexpression using flow cytometry. Data are presented as mean ± SD of three independent experiments. Statistical significance is indicated as follows: ** P < 0.05, *** P < 0.01, and *** P < 0.0001.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques: Over Expression, CCK-8 Assay, Cell Cycle Assay, Flow Cytometry

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: Partial rescue of proliferation inhibition and induction of apoptosis by E2F5 upregulation in AML cells overexpressing FOXN3. ( A ) Assessment of cell proliferation in leukemic cells co-transfected with lentiviruses for FOXN3 overexpression and E2F5 overexpression using the CCK-8 assay. ( B ) Flow cytometry analysis evaluated apoptosis in leukemic cells co-transfected with FOXN3 and E2F5 overexpressing lentiviruses. ( C ) Cell cycle analysis was performed on leukemic cells co-transfected with FOXN3 and E2F5 overexpressing lentiviruses using flow cytometry. Data are presented as mean ± SD of three independent experiments. Statistical significance is indicated as follows:* P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques: Inhibition, Transfection, Over Expression, CCK-8 Assay, Flow Cytometry, Cell Cycle Assay

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: Regulation of EZH2 and MAPK pathways by the FOXN3-E2F5 axis in AML. ( A ) Volcano plots illustrating differentially expressed genes in THP1 cells with FOXN3 overexpression compared to control THP1 cells. ( B ) The top twenty significant KEGG pathways related to differentially expressed genes in THP1 cells with FOXN3 overexpression compared to control THP1 cells. The red box highlights the signal pathway that are in agreement with the functional results. ( C ) Western blot analysis showing the protein levels of EZH2, ERK1/2, and phosphorylated ERK1/2 (p-ERK1/2) in cells co-transfected with lentiviruses for FOXN3 and E2F5 overexpression. The experiments were conducted using three independent replicates and the data are presented as mean ± SD. Statistical significance is indicated as follows: * P < 0.05, and ** P < 0.01.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques: Over Expression, Control, Functional Assay, Western Blot, Transfection

Journal: Blood and Lymphatic Cancer: Targets and Therapy

Article Title: Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy

doi: 10.2147/BLCTT.S571966

Figure Lengend Snippet: The mechanism of FOXN3-E2F5-EZH2-MAPK regulatory axis in AML.

Article Snippet: The primary antibodies used were as follows: FOXN3 (ab129453, 1:2500, Abcam, UK), E2F5 (A16042, 1:500, ABclonal, China), CDC42 (2466T, 1:1000, Cell Signaling Technology, MA), HDAC1 (34589T, 1:1000, Cell Signaling Technology, MA), PCNA (WL03213, 1:500, Wanleibio, China), CyclinE1 (WL01072, 1:1000, Wanleibio, China), CDK2 (WL01543, 1:500, Wanleibio, China), CyclinD1 (WL01435a, 1:400, Wanleibio, China), CDK6 (WL03460, 1:500, Wanleibio, China), Bcl-2 (WL01556, 1:1000, Wanleibio, China), EZH2 (WL00795, 1:1000, Wanleibio, China), p-ERK (WLP1512, 1:1000, Wanleibio, China), ERK (WL01864, 1:1000, Wanleibio, China), p-38 (WL00764, 1:1000, Wanleibio, China), and GAPDH (5174, 1:1000, Cell Signaling Technology, MA).

Techniques:

Journal: BMC Cancer

Article Title: E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer

doi: 10.1186/1471-2407-10-64

Figure Lengend Snippet: Clinical characteristics and age distribution of study samples (serum samples) used for E2F5 and CA125 expression studies.

Article Snippet: Primary antibodies directed against the AREB6 (AVIVA Systems Biology, San Diego, California, USA), E2F5 (Acris GmbH, Hiddenhausen, Germany), PAX8 (Abcam Limited, Cambridge, UK), and ELF3 (Orbigen Inc, San Diego, CA) were chosen as the four TFs suggested by the bioinformatics analysis.

Techniques: Expressing

Journal: BMC Cancer

Article Title: E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer

doi: 10.1186/1471-2407-10-64

Figure Lengend Snippet: Summary of Immunohistochemistry results for E2F5 antibody tested on OEC

Article Snippet: Primary antibodies directed against the AREB6 (AVIVA Systems Biology, San Diego, California, USA), E2F5 (Acris GmbH, Hiddenhausen, Germany), PAX8 (Abcam Limited, Cambridge, UK), and ELF3 (Orbigen Inc, San Diego, CA) were chosen as the four TFs suggested by the bioinformatics analysis.

Techniques: Immunohistochemistry

Journal: BMC Cancer

Article Title: E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer

doi: 10.1186/1471-2407-10-64

Figure Lengend Snippet: Validation of potential target (AREB6, PAX8, ELF3) using western blots (A) and expression of E2F5 in serum from normal, benign and, malignant patient samples (B) . (A) Target validation using western blots of AREB6, PAX8, ELF3, in serum of healthy volunteers (N) (n = 2), patients with benign ovarian cysts (B1, B2) (n = 2), and patients with late- (L1, L2) (n = 2) and early-stage (E1-E3) (n = 3) serous adenocarcinoma. AREB6 was overexpressed in late stage disease, but was not discriminatory for early cancer. PAX8 and ELF3 were equally expressed in all serum samples. (B) Expression of E2F5 in serum from normal (n = 56), benign (n = 40) and, malignant (n = 48) serum obtained from patients with cancer of the ovary.

Article Snippet: Primary antibodies directed against the AREB6 (AVIVA Systems Biology, San Diego, California, USA), E2F5 (Acris GmbH, Hiddenhausen, Germany), PAX8 (Abcam Limited, Cambridge, UK), and ELF3 (Orbigen Inc, San Diego, CA) were chosen as the four TFs suggested by the bioinformatics analysis.

Techniques: Biomarker Discovery, Western Blot, Expressing

Journal: BMC Cancer

Article Title: E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer

doi: 10.1186/1471-2407-10-64

Figure Lengend Snippet: Details of E2F5/CA125 expression pattern on different subtypes of OEC performed using western blotting technique.

Article Snippet: Primary antibodies directed against the AREB6 (AVIVA Systems Biology, San Diego, California, USA), E2F5 (Acris GmbH, Hiddenhausen, Germany), PAX8 (Abcam Limited, Cambridge, UK), and ELF3 (Orbigen Inc, San Diego, CA) were chosen as the four TFs suggested by the bioinformatics analysis.

Techniques: Expressing, Western Blot

Journal: BMC Cancer

Article Title: E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer

doi: 10.1186/1471-2407-10-64

Figure Lengend Snippet: Diagnostic accuracy developed for ovarian cancer detection with 13 features using Kstar classification based on SMOTE algorithms.

Article Snippet: Primary antibodies directed against the AREB6 (AVIVA Systems Biology, San Diego, California, USA), E2F5 (Acris GmbH, Hiddenhausen, Germany), PAX8 (Abcam Limited, Cambridge, UK), and ELF3 (Orbigen Inc, San Diego, CA) were chosen as the four TFs suggested by the bioinformatics analysis.

Techniques: Diagnostic Assay