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Image Search Results
Journal: Oncotarget
Article Title: Multiple direct and indirect mechanisms drive estrogen-induced tumor growth in high grade serous ovarian cancers
doi: 10.18632/oncotarget.6943
Figure Lengend Snippet: PEO1, NIH:OVCAR-3, COV318, and HEY cells were grown in complete culture medium and MCF-7 cells were used as positive control. A. The relative mRNA expression of hormone receptors was evaluated by RT-PCR, utilizing a specific sets of primers (see Table ). All samples were normalized to the housekeeping gene, GAPDH. The results are presented as fold change for each mRNA in HGSOC cell lines compared to MCF-7 cells. B. Representative Western blot of hormone receptors expressions. Protein levels were determined by subjecting 60 μg of protein extract to SDS-gel electrophoresis, followed by Western blotting using specific antibodies. β-actin was used as a control of equal sample loading.
Article Snippet: The ovarian carcinoma cell lines COV318 and PEO1 were purchased from the European Collection of Cell Cultures (ECACC, Salisbury, UK);
Techniques: Positive Control, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, SDS-Gel, Electrophoresis
Journal: Oncotarget
Article Title: Multiple direct and indirect mechanisms drive estrogen-induced tumor growth in high grade serous ovarian cancers
doi: 10.18632/oncotarget.6943
Figure Lengend Snippet: Cells were treated with various concentrations of substances in phenol-red free medium supplemented with charcoal stripped FBS. Concentrations are expressed in nanomolar. Control cells received the same amount of diluent. The medium was renewed after 48 hours. At 120 hours of incubation viable cells were counted using Nucleocounter. All results are expressed as the mean ± SEM derived from at least three different experiments. A. In PEO1 cells growth was modulated by E 2 or selective agonist treatment, an effect reverted by the ER antagonist ICI 182,780 (10 and 100 nM) (* P <0.05, ** P <0.01, *** P <0.001). To confirm the E 2 -induced modulation of cell proliferation, cyclin D1 and cyclin E was evaluated by western blot analysis after 120 hours treatment. Quantitated protein levels were normalized to β-actin (* P <0.05, ** P <0.01). B. The proliferation of NIH:OVCAR-3, COV318 and HEY was not modulated by either the endogenous or the selective synthetic ligands. MCF-7 cells were used as positive control.
Article Snippet: The ovarian carcinoma cell lines COV318 and PEO1 were purchased from the European Collection of Cell Cultures (ECACC, Salisbury, UK);
Techniques: Incubation, Derivative Assay, Western Blot, Positive Control
Journal: Oncotarget
Article Title: Multiple direct and indirect mechanisms drive estrogen-induced tumor growth in high grade serous ovarian cancers
doi: 10.18632/oncotarget.6943
Figure Lengend Snippet: A. E 2 stimulated the s.c. growth of NIH:OVCAR-3 compared to Ovx females (** P <0.01, n=8 mice/group). Histological features of the tumor (magnification 40x). B. Immunohistochemical analysis did not show any treatment-related difference in expression of the three ERβ isoforms (n=8 tumors/group). Nuc, nuclear and Cyt, cytoplasmic expression. C. Tumors in E 2 -treated females were characterized by a higher proliferative index (** P <0.01, n=8 tumors/group). Representative images for Ki67 immunostaining of tumors from Ovx and Ovx+E 2 mice (magnification 40x).
Article Snippet: The ovarian carcinoma cell lines COV318 and PEO1 were purchased from the European Collection of Cell Cultures (ECACC, Salisbury, UK);
Techniques: Immunohistochemical staining, Expressing, Immunostaining
Journal: Nature Communications
Article Title: Biomimetic organo-hydrogels reveal the adipose tissue local mechanical anisotropy regulates ovarian cancer invasion
doi: 10.1038/s41467-025-62296-7
Figure Lengend Snippet: a Schematic representation of adipose tissue-mimicking collagen-based organo-hydrogels (OHGs). b BODIPY (green) staining of human peritoneal adipose tissue and OHG (representative images from n = 7 patients and n = 3 OHGs). c Quantification of human peritoneal adipocyte ( n = 100 adipocytes/tissue from 7 patients) and silicone oil microdroplet ( n = 100 microdroplets from 3 OHGs) diameter. d Quantification of volume fraction occupied by oil in peritoneal adipose tissues ( n = 7 patients) and OHGs ( n = 3 gels). e Storage moduli of hydrogels and human peritoneal tissues ( n = 5 gels; n = 9 adipose and n = 5 connective tissues). f Normalised stress-relaxation curves of hydrogels and human peritoneal tissues ( n = 5 gels or tissues). g Spheroid area after 7 d relative to day 0 of multiple ovarian cancer cell lines ( n = 3 spheroids). h Spheroid area comparison of ovarian cancer cell lines after 7 d in collagen or OHGs relative to the collagen average ( n = 3 spheroids). i Collagen-I (grey) and mRFP-OVCAR8 nuclei (red) staining of OVCAR8 cells seeded on top of collagen or OHG at 25 μm gel depth after 7 d in culture (representative images from n = 3 experiments). j Quantification of hydrogel organotypic invasion of OVCAR8 cells after 7 d ( n = 3 experiments). Rhombuses indicate the average. k BODIPY (green), mRFP-OVCAR8 (red), and collagen I (grey) staining of peritoneal tissue explants and mRFP-OVCAR8 cells after 7 d in culture (representative images from n = 3 experiments). Arrowheads indicate invading mRFP-OVCAR8 cells. l Quantification of mRFP-OVCAR8 organotypic invasion into human peritoneal tissues after 7 d ( n = 3 tissues from distinct donors). Rhombuses indicate the average. m BODIPY (green) and mRFP (red) staining of mRFP-OVCAR8 cells in peritoneal tissue explants and OHGs (42 μm depth) after 7 d culture (representative images from n = 3 experiments). n Quantification of mRFP-OVCAR8 organotypic invasion into human peritoneal tissues or OHGs after 7 d ( n = 3 tissues from distinct donors or gels). Rhombuses indicate the average. For the data in ( c , d , g , h , j , l and n ), a two-sided unpaired t test was performed. One-way analysis of variance (ANOVA) with Tukey’s correction for multiple comparisons was performed for the data in ( e ). Error bars in ( e ) represent the s.e.m. Scale bars, 50 μm ( b , i , m ), 100 μm ( k ). Components of ( a ) have been created in BioRender. Gautrot, J. (2025) https://BioRender.com/rk3jchz . Source data are provided as a Source Data file.
Article Snippet: OVCAR3 (HTB-161, ATCC),
Techniques: Staining, Comparison
Journal: Nature Communications
Article Title: Biomimetic organo-hydrogels reveal the adipose tissue local mechanical anisotropy regulates ovarian cancer invasion
doi: 10.1038/s41467-025-62296-7
Figure Lengend Snippet: a pFAK, pMLC, YAP/TAZ (green; left to right) and nuclei (blue) staining of OVCAR8 cells in collagen or organo-hydrogel (OHG) after 48 h in culture (representative images from n = 3 gels). b Quantification of immunofluorescence signal intensity of cytoplasmic pFAK, pMLC, relative to the average in collagen and cytoplasmic:nuclear ratio of YAP/TAZ in OVCAR8 cells embedded in collagen or OHG for 48 h ( n = 24 cells). c F-actin (yellow), nucleus (blue) and BODIPY (grey) staining of an OVCAR8 cell spread at the ECM-microdroplet interface. d Shape descriptors of OVCAR8 nuclei after 24 h in collagen or OHG ( n = 53 nuclei). e Relative spheroid area of OVCAR8 after 7 d in OHG ( n = 10 spheroids). f BODIPY (green) and mRFP (red) staining of peritoneal adipose tissue explants and mRFP-OVCAR8 cells (49 μm into the tissue from the surface) after 7 d in culture (representative images from n = 3 experiments). g Quantification of mRFP-OVCAR8 organotypic invasion into human peritoneal tissues after 7 d ( n = 3 tissues from distinct donors). Rhombuses indicate the average. h Nuclei (red) of OVCAR8 cells in OHGs after 7 d treatment (representative images from n = 14 spheroids). i Quantification of spheroid area relative to DMSO control of OVCAR8 cells in OHGs ( n = 14 spheroids). i F-actin (green) and nuclei staining of CAOV3 spheroids embedded in OHGs for 7 d (representative images from n = 6 spheroids). k Quantification of spheroid area in CAOV3 cells in OHGs after 7 d ( n = 6 spheroids). l F-actin (green) and nuclei (blue) staining of Kuramochi spheroids in collagen or OHG for 7 d with or without TGFβ (representative images from n = 3 spheroids). For the data in ( b , d , g , i and k ), a two-sided unpaired t test was performed. For data in ( e ), a one-way analysis of variance (ANOVA) with Tukey’s correction for multiple comparisons was performed. Scale bars, 25 μm ( a , c ), 100 μm ( f , I ), 200 μm ( h , j ). Source data are provided as a Source Data file.
Article Snippet: OVCAR3 (HTB-161, ATCC),
Techniques: Staining, Immunofluorescence, Control
Journal: Nature Communications
Article Title: Biomimetic organo-hydrogels reveal the adipose tissue local mechanical anisotropy regulates ovarian cancer invasion
doi: 10.1038/s41467-025-62296-7
Figure Lengend Snippet: a Schematic representation of norbornene-functionalised hyaluronic acid (NB-HA)-based organohydrogels (OHGs) presenting matrix metalloproteinase (MMP)-degradable crosslinking peptides and cell adhesion ligands. b Storage moduli of collagen- and NB-HA-based OHGs ( n = 5 collagen-based and n = 3 NB-HA-based OHGs; average ± s.e.m.). c Normalised stress-relaxation curves of collagen- and HA-NB OHG ( n = 5 collagen-based and n = 3 NB-HA-based OHGs). d F-actin (grey) and nuclei (red) in OVCAR8 cells embedded in collagen- or NB-HA-based OHGs for 7 d (representative images from n = 9 spheroids). e OVCAR8 spheroid area in collagen- or NB-HA-based OHGs relative to collagen-based OHG average ( n = 9 spheroids). f F-actin (grey) and nuclei (red) of OVCAR8 cells embedded in GFOGER- or RGD-presenting NB-HA OHG (representative images from n = 9 spheroids). g BODIPY (green), nuclei (red), and F-actin (grey) of OVCAR8 in GFOGER- or RGD-presenting NB-HA OHG (representative images from n = 9 spheroids). Arrowheads indicate cells in direct contact with oil microdroplets. h OVCAR8 spheroid area in GFOGER- or RGD-presenting NB-HA OHG after 7 d culture relative to GFOGER OHG average ( n = 9 spheroids). i F-actin (grey) and nuclei (red) in OVCAR8 cells embedded in collagen-based OHGs for 7 d (representative images from n = 8 spheroids). j OVCAR8 spheroid area in collagen-based OHGs after 7 d culture relative to DMSO control ( n = 8 spheroids). k BODIPY (green) and mRFP (red) staining of peritoneal adipose tissue explants and mRFP-OVCAR8 cells. l Quantification of mRFP-OVCAR8 organotypic invasion depth into human peritoneal tissues after 7 d ( n = 3 tissues from distinct donors). Rhombuses indicate the average. m OVCAR8 spheroid area quantifications in MMP-cleavable or non-cleavable NB-HA OHG after 7 d culture relative to MMP-cleavable control ( n = 11 spheroids). For the data in ( b , e , h , j and l ), a two-sided unpaired t test was performed. One-way analysis of variance (ANOVA) with Tukey’s correction for multiple comparisons was performed for the data in ( m ). Error bars in ( b ) represent the s.e.m. Scale bars, 100 μm ( g , k ), 200 μm ( d , f , i ). Source data are provided as a Source Data file.
Article Snippet: OVCAR3 (HTB-161, ATCC),
Techniques: Control, Staining
Journal: Nature Communications
Article Title: Biomimetic organo-hydrogels reveal the adipose tissue local mechanical anisotropy regulates ovarian cancer invasion
doi: 10.1038/s41467-025-62296-7
Figure Lengend Snippet: a F-actin (grey) and DAPI (blue) in OVCAR8 cells embedded in collagen or collagen-based organo-hydrogels (OHG) for 24 h (representative images from n = 3 gels). Microdroplet locations are indicated with an asterisk. b BODIPY (green), F-actin (grey) and nuclei (blue) staining of OVCAR8 cells embedded in collagen-based OHG (left; n = 3 gels) or BODIPY (green), mRFP (red) staining of mRFP-OVCAR8 cells invading into peritoneal adipose tissue (right; n = 3 tissues from 1 donor). Arrowheads indicate oil microdroplet (left) and adipocyte (right) deformations at the contact points with cells. c Quantification of OVCAR8 organotypic invasion depth into peritoneal adipose tissues after 7 d ( n = 3 tissues from 1 donor). Rhombuses indicate the average. d Schematic representation of the Sylgard 184 PDMS-based OGH. e F-actin (grey) and nuclei (red) staining of OVCAR8 spheroids embedded for 7 d in collagen-based OHGs prepared with PDMS microdroplets of varying stiffness (representative images from n = 10 spheroids). f OVCAR8 spheroid area after 7 d in collagen-based OHGs with PDMS microdroplets prepared with varying crosslinker percentage, relative to average area in 2 wt% microbead OHGs ( n = 10 spheroids). g Schematic representation of the norbornene-functionalised hyaluronic acid (NB-HA) OGH with norbornene-functionalised bovine serum albumin (NB-BSA) used for RGD presentation at the microdroplet surface. h F-actin (grey) and nuclei (red) of OVCAR8 spheroids after 7 d in NB-HA OHG with localised presentation of RGD (left). Relative OVCAR8 spheroid area in NB-HA OHG with localised RGD presentation after 7 d in culture ( n = 11 spheroids; top right). BODIPY (green), nuclei (red), and F-actin (grey) staining of OVCAR8 cells in NB-HA OHG presenting RGD on the microdroplet surface (bottom right). Arrowhead indicates a cell spreading at the microdroplet-HA interface. i Schematic representation of the system to modulate microdroplet interfacial mechanics. j F-actin (grey) and nuclei (red) of OVCAR8 spheroids after 7 d in NB-HA OHGs (microdroplet-restricted RGD presentation) with varying microdroplet interfacial modulus (representative images from n = 9 spheroids). k OVCAR8 spheroid area in NB-HA OHGs with microdroplet-presenting RGD and varying protein nanosheet interfacial mechanics after 7 d in culture, relative to BSA-only control ( n = 9 spheroids). For the data in ( c and h ), a two-sided unpaired t test was performed. One-way analysis of variance (ANOVA) with Tukey’s correction for multiple comparisons was performed for the data in ( f and k ). Scale bars, 25 μm ( a , b ), 50 μm ( h , bottom right), 200 μm ( e , h left, j ). Source data are provided as a Source Data file.
Article Snippet: OVCAR3 (HTB-161, ATCC),
Techniques: Staining, Control
Journal: Nature Communications
Article Title: Biomimetic organo-hydrogels reveal the adipose tissue local mechanical anisotropy regulates ovarian cancer invasion
doi: 10.1038/s41467-025-62296-7
Figure Lengend Snippet: a Schematic representation of the organo-hydrogels (OHGs) with varying microdroplet diameter and volume fraction. b Storage modulus of collagen-based OHG with distinct microdroplet size ( n = 4 gels; average ± s.e.m.). The dashed line shows the predicted trend. c Normalised stress-relaxation curves of collagen-based OHG with distinct microdroplet size ( n = 4 gels). d BODIPY (green) and F-actin (red) and nuclei (blue) staining of OVCAR8 cells after 7 d in collagen-based OHG of 70 or 25 μm diameter microdroplets (representative images from n = 13 spheroids). Arrowheads indicate cells at the invasive front. e Quantification of relative OVCAR8 spheroid area in collagen-based OHG of distinct emulsion percentage of volume fraction and microdroplet diameter after 7 d in culture ( n = 13 spheroids). f BODIPY (green) and mRFP (red) staining of mRFP-OVCAR8 cells after 7 d invasion into adipose peritoneal tissue explants (representative images from n = 3 explants per donor). g Correlation between patient average adipocyte diameter and invaded OVCAR8 cells after 7 d, at 42 μm tissue depth, relative to number of cells at the tissue surface ( n = 6 donors; average ± s.e.m.). The dashed line shows the predicted trend. h Quantification of interdroplet distance in OHG ( n = 100 microdroplets). i Quantification of the percentage of invasive front OVCAR8 cells in contact with microdroplets in OHG ( n = 121 cells in 3 gels). j Quantification of percentage of Ki67 + cells, immunofluorescence signal intensity of cytoplasmic pFAK and pMLC relative to collagen average, and nuclear:cytoplasmic ratio of YAP/TAZ in OVCAR8 cells embedded in OHG of 70 or 25 μm diameter microdroplets for 24 h ( n = 55 cells). k F-actin (green) and DAPI (blue) staining of CAOV3 spheroids embedded for 7 d in collagen-based 25 μm microdroplet OHG in the presence or absence of TGFβ. Arrowheads indicate invading cells (representative images from n = 6 spheroids). l Quantification of CAOV3 spheroid area relative to non-TGFβ-treated control after 7 d in culture ( n = 6 spheroids). m Schematic illustration of the cell force-dependent invasion of adipose tissue enabled by the anisotropic mechanics of OHGs and the generation of migration tracks at the ECM-adipocyte/microdroplet interface. Arrows indicate the direction of the force. For the data in ( h , i , j and l ), a two-sided unpaired t test was performed. Coefficient of determination and Pearson correlation (two-tailed test) were performed in ( g ) to determine the relationship between tissue adipocyte diameter and OVCAR8 invasion. Error bars in ( b ) represent the s.e.m. Scale bars, 50 μm (bottom panels in d , k ), 100 μm ( f ), 200 μm (top panels in d , k ). Source data are provided as a Source Data file.
Article Snippet: OVCAR3 (HTB-161, ATCC),
Techniques: Staining, Emulsion, Immunofluorescence, Control, Migration, Two Tailed Test
Journal: Frontiers in Oncology
Article Title: SIRT6 Is Involved in the Progression of Ovarian Carcinomas via β-Catenin-Mediated Epithelial to Mesenchymal Transition
doi: 10.3389/fonc.2018.00538
Figure Lengend Snippet: The effect of SIRT6 on the proliferation and invasiveness of ovarian cancer cells. (A) Counting the number of cells, MTT, BrdU incorporation, and colony forming assays were performed to evaluate the proliferation of OVCAR3 and OVCAR5 ovarian cancer cells after knock-down of SIRT6 with shRNA for SIRT6 or overexpression of SIRT6 with wild-type SIRT6. Western blotting was performed to show knock-down or overexpression of SIRT6. (B) Migration and invasion assays were performed to evaluate the invasiveness of OVCAR3 and OVCAR5 cells after knock-down of SIRT6 or overexpression of SIRT6. The number of cells which migrated or invaded the chambers were counted in five microscopic fields per well at one-hundred magnification. (C) Western blotting was performed for SIRT6, β-catenin, active β-catenin, snail, vimentin, MMP9, MMP2, N-cadherin, E-cadherin, and actin after knock-down of SIRT6 or overexpression of SIRT6 in OVCAR3 and OVCAR5 cells. The western bands were quantified using ImageJ software and values are indicated below the bands. (D) Quantitative reverse-transcription polymerase chain reaction was performed for SIRT6, β-catenin, snail, vimentin, MMP9, MMP2, N-cadherin, and E-cadherin after knock-down of SIRT6 or overexpression of SIRT6 in OVCAR3 and OVCAR5 cells. CV, control vector; OE, overexpression; *, vs. control; P < 0.05.
Article Snippet:
Techniques: BrdU Incorporation Assay, Knockdown, shRNA, Over Expression, Western Blot, Migration, Software, Reverse Transcription, Polymerase Chain Reaction, Control, Plasmid Preparation
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Comparison of changes induced by knockout of CDR1 , CDR2 , and CDR2L in the transcriptome, proteome, and secretome of ovarian cancer cells. (A) Venn diagram showing the number of genes identified in each dataset and the overlap between datasets. (B) The proportion of differentially expressed genes (y-axis) for each knockout cell line (colour) per dataset (x-axis). The percentage was calculated based on the number of genes in each pre-filtered dataset. (C) Upset plots where the rows correspond to the significantly (FDR < 0.05) differentially expressed genes in each knockout cell line, and the columns correspond to the intersecting genes in each dataset (panels). The orange bar highlights the number of differentially expressed genes common to all cell lines. The dark blue bar highlights differentially expressed genes unique to CDR2L -knockout cells. (D) Principal component plot. Datapoints represent samples in the first (x-axis) and second (y-axis) principal component space. Color-coding indicates group variable. Analysis was performed separately on each dataset (panels)
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Comparison, Knock-Out
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Gene set enrichment analysis of mRNAs and proteins with expression altered by CDR2L knockout. A-C , The top 30 (sorted by significance) up- and downregulated GO and KEGG gene sets in (A) transcriptome, (B) proteome, and (C) secretome of CDR2L -knockout cells. The gene sets were collapsed to reduce redundancy in the results. The horizontal axis represents the positive (orange) and negative (blue) normalized enrichment scores. The transparency of the bars reflects significance (at FDR < 0.05). (D) Heatmap of enriched pathways common to at least two datasets. The columns correspond to enriched GO and KEGG pathways, rows correspond to omic datasets. The colour and transparency of each cell represents the direction of the normalized enrichment scores (NES) and the significance, respectively
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Expressing, Knock-Out
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Ribosome biogenesis factors are affected differently in the transcriptome and proteome of CDR2L - knockout cells. Heatmap of differentially expressed genes from the GO term “ribosome biogenesis” detected in the transcriptome and proteome of CDR2L -knockout cells. The columns correspond to the datasets, and the rows correspond to individual genes. The colour of each cell represents the direction of the log2 fold change. The annotations on the left side of the heatmap describe whether the gene is significantly differently expressed, and the annotations on the right side indicate the step in the ribosome biogenesis pathway with which the gene is associated
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Knock-Out
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Knockout of CDR2L affects cell cycle-related pathways. (A) GO terms from the gene set enrichment analysis of the proteome of CDR2L -knockout cells visualized as a functionally organized network. Node colours represent grouped pathway terms. Group titles were chosen by selecting the most significant term in that group. Node shape represents the database source: circle, GO biological process; hexagon, GO molecular function; and square, GO cellular component. Significance of each pathway is reflected by the node size, with a larger shape representing a higher significance. Term-term interactions are shown as edges in the network where the thickness of the edge represents the extent of overlap. Only groups with more than two nodes are shown. (B) Heatmap of selected cell cycle-related genes significantly differentially expressed (FDR < 0.05) in both transcriptome and proteome of CDR2L -knockout cells. The columns correspond to the datasets, and the rows correspond to individual genes. The colour of each cell represents the direction of the log2 fold change. CDKs, cyclin-dependent kinases; CDKIs, cyclin-dependent kinase inhibitors; MCM, minichromosome maintenance
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Knock-Out
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Comparison and correlational analysis between the transcriptome and proteome of CDR2L -knockout cells. (A) Venn diagram showing the number of shared and unique differentially expressed genes between the transcriptome and proteome of CDR2L -knockout cells. (B) Scatter plot showing log2 fold change of all genes significantly differentially expressed (FDR < 0.05) in both transcriptome (x-axis) and proteome (y-axis; n = 1958). The colour represents the four groups of possible combinations of direction of change. Correlation between log2 fold changes in transcriptome and proteome was assessed using Spearman’s rank correlation
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Comparison, Knock-Out
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Protein-protein interaction networks of genes altered in both transcriptome and proteome of CDR2L -knockout cells. Genes significantly differentially expressed (FDR < 0.05) in both the transcriptome and proteome of CDR2L -knockout cells were used to create a protein-protein interaction network in STRING. The network was subsequently clustered using Markov clustering to identify clusters of tightly connected genes. Each node represents a gene, and the colour indicates down- (blue) or upregulation (red). Inner rings represent transcriptome data and outer rings represent proteome data. Clusters with > = 10 nodes are shown along with their most significant enriched GO biological process terms (FDR < 0.05)
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Knock-Out
Journal: BMC Cancer
Article Title: Multi-omics profiling reveals dysregulated ribosome biogenesis and impaired cell proliferation following knockout of CDR2L
doi: 10.1186/s12885-024-12399-z
Figure Lengend Snippet: Analysis of WT and CDR2L -knockout ovarian cancer cell proliferation in vitro. The proliferation rate of wild-type (WT) OVCAR-3 cells and CDR2L -knockout cells was evaluated by live cell imaging. Plotted is the time in hours (x-axis) versus confluency calculated as a percentage of the surface of the imaged wells (y-axis). The data is presented as means with standard errors
Article Snippet: CDR1 -knockout, CDR2 -knockout, and
Techniques: Knock-Out, In Vitro, Live Cell Imaging