eac cell line oe33  (China Center for Type Culture Collection)

Journal: Pharmaceutics

Article Title: Harnessing Nature for Breast Cancer Management: Effects of Fisetin-Loaded Nigellasomes Embedded in Microneedles Improve Tumor Suppression and Reduce Oxidative Stress

doi: 10.3390/pharmaceutics17111392

Figure Lengend Snippet: Schematic representation of the in vivo study utilizing breast cancer using Ehrlich model.

Article Snippet: The Ehrlich Ascites Carcinoma (EAC) cell line (ATCC CCL-77) was generously provided by the Pharmacology and Experimental Oncology Unit of the National Cancer Institute at Cairo University in Egypt.

Techniques: In Vivo

Journal: Pharmaceutics

Article Title: Harnessing Nature for Breast Cancer Management: Effects of Fisetin-Loaded Nigellasomes Embedded in Microneedles Improve Tumor Suppression and Reduce Oxidative Stress

doi: 10.3390/pharmaceutics17111392

Figure Lengend Snippet: ( a ). Skin morphology and tumor volume in model induced by Ehrlich in different groups. ( b – f ) Effects of different treatments on inflammatory biomarkers measured by ELISA: ( b ) NLRP3, ( c ) TNF-α, ( d ) IL-1β, ( e ) NF-κB, and ( f ) mTOR. ( g ) Lipid peroxidation (LPO, expressed as MDA levels). ( h – j ) Antioxidant activities: ( h ) catalase, ( i ) superoxide dismutase (SOD), and ( j ) glutathione (GSH). Data are expressed as mean ± SD (n = 10). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, and ns (not significant) versus the control group. Abbreviations: Group I (normal group, negative control), Group II (disease model group, positive control), Group III (treated with FIS loaded with gel containing 2% ( w / w ) HPMC), Group IV (treated with FIS-NSs loaded with gel containing 2% ( w / w ) HPMC), Group V (FIS-NSs-loaded G/HA/CMC MNs).

Article Snippet: The Ehrlich Ascites Carcinoma (EAC) cell line (ATCC CCL-77) was generously provided by the Pharmacology and Experimental Oncology Unit of the National Cancer Institute at Cairo University in Egypt.

Techniques: Enzyme-linked Immunosorbent Assay, Control, Negative Control, Positive Control

Journal: Pharmaceutics

Article Title: Harnessing Nature for Breast Cancer Management: Effects of Fisetin-Loaded Nigellasomes Embedded in Microneedles Improve Tumor Suppression and Reduce Oxidative Stress

doi: 10.3390/pharmaceutics17111392

Figure Lengend Snippet: ( a ) Histopathological features of H&E staining dissected sections of Solid Ehrlich Carcinoma (SEC) tissues with ×100 magnified images, assessing the effect of fisetin formulation. Photomicrographs show aggregates of high number of neoplastic cells with mitotic figures (black arrows) surrounded by moderate areas of necrotic tissues (star) (Hematoxylin and Eosin staining). Effects of formulations on the average number of mitotic cells ( b ) and the average number of giant tumor cells ( c ). Data are expressed as mean ± SD (n = 10). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 versus the control group. Note : GI (healthy negative control group), GII (SEC model group, untreated), GIII (treated with fisetin incorporated in gel containing 2% ( w / w ) HPMC), GIV (treated with Fisetin– Nigella sativa nanovesicles incorporated in gel containing 2% ( w / w ) HPMC), GV (treated with Fisetin– Nigella sativa nanovesicles incorporated in G/HA/CMC microneedles).

Article Snippet: The Ehrlich Ascites Carcinoma (EAC) cell line (ATCC CCL-77) was generously provided by the Pharmacology and Experimental Oncology Unit of the National Cancer Institute at Cairo University in Egypt.

Techniques: Staining, Formulation, Control, Negative Control

Journal: Cell Death & Disease

Article Title: AKR1C3 enhances radioresistance in esophageal adenocarcinoma via inhibiting ferroptosis through suppressing TRIM21-mediated ubiquitination of HSPA5

doi: 10.1038/s41419-025-07773-z

Figure Lengend Snippet: A Proteomic analysis was conducted on the immunoprecipitated products from anti-AKR1C3 co-IPs of OE33 AKR1C3 and SKGT-4. Venn diagram exhibited the integration of proteomic results with 234 ferroptosis suppressors. Totally 13 enriched genes were listed. B Co-IP assay results presented the interactions between AKR1C3 and HSPA5 in EAC cells. C Immunofluorescence assay results showed the co-localization of AKR1C3 with HSPA5 in EAC cells. D Western blot results exhibited the protein expression of HSPA5, AKR1C3, and GPX4 in different EAC cell lines. E Western blot results exhibited ubiquitin level of HSPA5 in different EAC cell lines. F Western blot results showed the protein level of HSPA5 with or without MG-132 treatment in SKGT-4 shNT/shAKR1C3 cell lines. G Proteomic analysis was conducted on the immunoprecipitated products from anti-HSPA5 co-IPs of OE33 AKR1C3 and SKGT-4. Venn diagram exhibited the integration of proteomic results with 377 E3 ubiquitin ligases. TRIM21 was enriched. H Co-IP assay results presented the interactions between TRIM21 and HSPA5 in EAC cells. I Co-IP assay results presented the different strengths of interactions between TRIM21 and HSPA5 in EAC cells. J Analyses of HSPA5 binding domains with AKR1C3. Four truncated forms of HA-HSPA5 were individually co-transfected with Flag-tagged AKR1C3 into HEK293T cells, and co-IP was performed with the anti-HA antibody.

Article Snippet: The human EAC cell line SKGT-4 was obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany), OE33 was obtained from the Sigma Cell Line Bank (Sigma, #96070808, Germany).

Techniques: Immunoprecipitation, Co-Immunoprecipitation Assay, Immunofluorescence, Western Blot, Expressing, Ubiquitin Proteomics, Binding Assay, Transfection

Journal: bioRxiv

Article Title: Esophageal adenocarcinoma relapse after chemoradiation is dominated by a basal-like subtype

doi: 10.1101/2025.01.28.635332

Figure Lengend Snippet: RCT treatment response tested in three EAC models. (A) Cell Titer Glo (CTG) viability assay illustrates the distinct responses of Eso26, OE19, and OEx33 esophageal adenocarcinoma (EAC) cell lines to RCT treatment. CROSS chemotherapeutic concentrations displayed on the x-axis are calculated as µM Carboplatin and µM*10 Paclitaxel concentrations combined with 2 Gy of radiation. (B) Experimental design and workflow for in vivo -based analyses. (C) Overview of the combined RCT treatment protocol executed in vivo . (D) Graphical representation of growth curves for the three EAC tumor models, showcasing the initial response to RCT treatment and subsequent post-treatment progression in 4 out of 13 tumors in the OE33x model, 4 out of 6 tumors in the OE19 model, and in 6 of 8 tumors in the Eso26 model following RCT treatment. FFPE refers to formalin-fixed, paraffin-embedded tissue; N, numbers of tumors included in the analysis. (E) Growth rates of three EAC xenograft models before and at day 40 after RCT start. ***, P < 0.001 T-test.

Article Snippet: Human EAC cell lines Eso26, OE19 and OE33 were obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany).

Techniques: Viability Assay, In Vivo, Formalin-fixed Paraffin-Embedded

Journal: bioRxiv

Article Title: Esophageal adenocarcinoma relapse after chemoradiation is dominated by a basal-like subtype

doi: 10.1101/2025.01.28.635332

Figure Lengend Snippet: Reduced function of BRCA2 leads to changes in migration potential and DNA damage response in EAC tumor cell models. (A) CRISPR/Cas9 mediated BRCA2 allele alteration was induced in 120 clones across three EAC cell lines. The resulting clones were verified through Sanger sequencing. Notably, none of the viable BRCA2 edited clones had a homozygous BRCA2 knockout (KO). The BRCA2 edited clones have one wild type/in-frame BRCA2 allele left, referred to as BRCA2 kd. (B) Verification of BRCA2 kd across EAC models through Western blot analysis. (C) Top: OE19 BRCA2 kd cells exhibit enhanced migration rates, as assessed through a wound-healing assay, in comparison to parental cells at 0, 24, and 48 hours (* P<0.05, T-test). Bottom: ImageJ analysis of inverted microscopic measurements were employed to measure the distance traveled by cells. (D) Immunofluorescence staining of γH2AX in Eso26 parental and BRCA2 kd cells. The expression of the DNA damage marker γH2AX increased in 50 µM Carboplatin-treated Eso26 BRCA2 kd tumors compared to parental tumors 40x magnification. CPT, Carboplatin. (E) Xenograft growth dynamics in parental and BRCA2 kd tumors. BRCA2 kd significantly decreased the tumor growth potential in vivo when compared to parental tumors. (F) Growth rates of three EAC parental and BRCA2 kd xenograft models. *, P<0.05 T-test.

Article Snippet: Human EAC cell lines Eso26, OE19 and OE33 were obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany).

Techniques: Migration, CRISPR, Clone Assay, Sequencing, Knock-Out, Western Blot, Wound Healing Assay, Comparison, Immunofluorescence, Staining, Expressing, Marker, In Vivo

Journal: bioRxiv

Article Title: Esophageal adenocarcinoma relapse after chemoradiation is dominated by a basal-like subtype

doi: 10.1101/2025.01.28.635332

Figure Lengend Snippet: Induced genomic response in EAC parental and BRCA2 kd tumors post RCT treatment. (A) Genomic copy number analysis based on WES defines the genomic instability index (GII, y-axis) as a measure for the fraction of the genome that is altered. RCT treatment induces GII to a moderate extent while BRCA2 kd leads to high GII in Eso26 and OE19 tumor models. (B) Single nucleotide variant (SNV) analysis of mutations acquired during the course of the experiment compared to parental cell lines without treatment reveals three mutation signatures. (C) Copy number profile of chromosome 19 (y-axis) of post-RCT relapsed Eso26 tumors and parental Eso26 as reference is shown with red indicating gained copy number. Note consistent copy number gain of chromosome 19q in Eso26 RCT-treated tumors compared to treatment-naive tumors. Known cancer-related genes are shown on the right.

Article Snippet: Human EAC cell lines Eso26, OE19 and OE33 were obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany).

Techniques: Variant Assay, Mutagenesis

Journal: bioRxiv

Article Title: Esophageal adenocarcinoma relapse after chemoradiation is dominated by a basal-like subtype

doi: 10.1101/2025.01.28.635332

Figure Lengend Snippet: Transcriptomic and proteomic profile changes are most prominent in BRCA2 kd tumor models. (A) Hierarchical clustering of the Euclidean distance matrix based on 3’ mRNASeq normalized gene expression of the three EAC tumor models. This heatmap showing sample similarity and the dominant signature of EAC cell lines. (B) Hierarchical clustering of the Euclidean distance matrix based on proteomic data of the three EAC tumor models. Heatmap illustrates proteins that are differentially expressed across all groups in the EAC tumor models.

Article Snippet: Human EAC cell lines Eso26, OE19 and OE33 were obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany).

Techniques: Gene Expression

Journal: bioRxiv

Article Title: Esophageal adenocarcinoma relapse after chemoradiation is dominated by a basal-like subtype

doi: 10.1101/2025.01.28.635332

Figure Lengend Snippet: BRCA2 kd and RCT treatment induced overlapping transcriptomic changes in EAC tumor models. (A) Illustration depicting the numbers of DEGs across the three EAC tumor models. (B) Correlation analysis of gene expression differences between RCT-treated vs. untreated Eso26 tumors (x-axis) and untreated OE19 vs. Eso26 tumors (y-axis). (C) Correlation analysis of gene expression differences between RCT-treated vs. untreated Eso26 tumors and untreated Eso26 BRCA2kd vs. untreated Eso26 parental tumors. (D) Definition of resistance expression signature based on common expression differences between Eso26 treated vs. untreated and OE19 vs. Eso26 (left schematic and left and middle column in heatmap). Resistance gene set of 48 genes correlates with transcriptomic changes induced by BRCA2 kd in Eso26 (right column in heatmap). (E) GSEA for REACTOME pathways for differentially expressed genes between Eso26 RCT vs. Eso26 parental. (F) Correlation analysis between gene expression differences of RCT treated Eso26 vs. untreated tumors and the basal-like keratinization vs. classic subtype reported by Guo et al. 2018 .

Article Snippet: Human EAC cell lines Eso26, OE19 and OE33 were obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany).

Techniques: Gene Expression, Expressing

Journal: bioRxiv

Article Title: Esophageal adenocarcinoma relapse after chemoradiation is dominated by a basal-like subtype

doi: 10.1101/2025.01.28.635332

Figure Lengend Snippet: Elevated expression of basal cell marker keratin 6 (KRT6) is associated with poor survival in EAC patients who underwent neoadjuvant treatment. (A) Gene expression heatmap shows the overexpression of several keratins in RCT-treated Eso26 tumors. (B) Immunohistochemical (IHC) staining of KRT6 in a tumor with (RCT) and without treatment (Ctrl) shows overexpression of KRT6 in treated Eso26 tumors. (C) Examples for KRT6 expression levels low and high for the analysis of tissue microarray (TMA) by IHC showing the differential expression levels of KRT6 in EAC patient tumors. . (D) Quantitative analysis of KRT6 IHC of 1161 EACs from Cologne arranged as TMA. Zero represents KRT6 negative, low indicates <25% KRT6 positive, and high signifies >25% KRT6 positive tumor cells. (E) Kaplan-Meier survival analysis of 728 EAC patients with evaluable IHC and survival data with different levels of KRT6 expression. Analysis of all patients is shown on top (HR = 1.201; 95%CI = 1.032 - 1.397), treatment naive patients (middle; HR = 1.189; 95%CI = 0.8977 - 1.574), and EAC of patients post-treatment at the bottom (HR = 1.202; 95%CI = 1.002 - 1.442).

Article Snippet: Human EAC cell lines Eso26, OE19 and OE33 were obtained from Deutsche Sammlung von Mikroorganismen und Zellkulturen (DSMZ, Germany).

Techniques: Expressing, Marker, Gene Expression, Over Expression, Immunohistochemical staining, Immunohistochemistry, Microarray, Quantitative Proteomics

Journal: Gastro Hep Advances

Article Title: The Involvement of Oral Pathogenic Bacteria, Fusobacterium nucleatum Subspecies animalis in the Pathogenesis of Human Esophageal Adenocarcinoma

doi: 10.1016/j.gastha.2025.100660

Figure Lengend Snippet: Influence of bacterial supernatant on EAC cells. (A) Representative images of EAC cells (OE33 cells) treated with each bacterial supernatant. Prevotella intermedia (Pi), F . nucleatum spp. nucleatum (Fnn), F . nucleatum spp. animalis (Fna) P . gingivalis (Pgin). Treatment with Gifu Anaerobic Medium was set as a negative control. (B) Relative expression of inflammatory cytokine or chemokine genes in EAC cells cultured with the bacterial conditioned media. β-actin was used as an internal control. (C-D) Immunofluorescence images of 53BP1 and γH2AX staining (C) and the number of γH2AX- and 53BP1-double positive foci per cell (D). Scale bar, 10 μm. (E-F) Representative images (E) and olive tail moment (F) in neutral comet assay. In (D) and (F), n = 50 in each group. In each assay, OE33 cells were treated with a 1/100 dilution of bacterial supernatant for 3 days, and treatment with Gifu Anaerobic Medium was set as a negative control. Data were obtained by 3 or more biological independent experiments. In all dot plots, error bars indicate mean ± standard deviation.

Article Snippet: The EAC cell line OE33 was obtained from AddexBio (Shanghai, China).

Techniques: Negative Control, Expressing, Cell Culture, Control, Immunofluorescence, Staining, Neutral Comet Assay, Standard Deviation

Journal: Gastro Hep Advances

Article Title: The Involvement of Oral Pathogenic Bacteria, Fusobacterium nucleatum Subspecies animalis in the Pathogenesis of Human Esophageal Adenocarcinoma

doi: 10.1016/j.gastha.2025.100660

Figure Lengend Snippet: Fusobacterium nucleatum spp. animalis provokes DNA damage in EAC cells through ROS accumulation. (A-B) Detection of intracellular ROS in cells cultured with bacterial conditioned medium. F . nucleatum spp. nucleatum (Fnn), F . nucleatum spp. animalis (Fna). Treatment with GAM was set as a negative control. ROS was stained by the CellROX DeepRed reagent, and representative fluorescent microscopic images (A) and their mean fluorescence intensity per cell (B) are shown. Scale bar, 50 μm. (C-D) DNA damage foci in cells treated with and without N-Acetyl-L-cysteine. OE33 cells were treated with either GAM medium or supernatant of F. nucleatum spp. animalis (Fna) with and without 5 mM N-Acetyl-L-cysteine. Representative images (C) and the number of γH2AX- and 53BP1-double positive foci per cell (D) are shown. Scale bar, 10 μm. In (B), n = 50 in each group, and in (D), n = 60 in each group. In each assay, OE33 cells were treated with a 1/100 dilution of bacterial supernatant for 3 days, and treatment with GAM was set as a negative control. Data were obtained by 3 or more biological independent experiments. In all dot plots, error bars indicate mean ± standard deviation. GAM, Gifu Anaerobic Medium.

Article Snippet: The EAC cell line OE33 was obtained from AddexBio (Shanghai, China).

Techniques: Cell Culture, Negative Control, Staining, Fluorescence, Standard Deviation