ovcar 3  (ATCC)

Journal: bioRxiv

Article Title: Systems serology of responses against tumor antigens in ovarian cancer reveal disrupted Fc-mediated immunity

doi: 10.64898/2026.04.25.720834

Figure Lengend Snippet: A) Quantification of Cetuximab, an IgG1 Ab, binding to OVCAR3 cells as compared to patient TBAs by fluorescence. Cetuximab was incorporated at concentrations of 0.01–0.1 µg/mL. B) Quantification of Cetuximab binding to FcγRIIIa as compared to patient TBAs via fluorescence. C) Percent cytotoxicity of unmodified patient TBAs, quantified by an in vitro effector response assay (n=36). All patient TBAs were normalized to the same concentration. Cetuximab was used as a positive control (+). NK cells co-incubated with OVCAR3 cells alone functioned as the negative control (-). A purple bar indicates a patient that was evaluated in A) and B). Data are represented as average ± standard deviation. See also Figure S4.

Article Snippet: OVCAR3 cells (ATCC HTB-161) were grown in complete growth media.

Techniques: Binding Assay, Fluorescence, In Vitro, Concentration Assay, Positive Control, Incubation, Negative Control, Standard Deviation

Journal: Cell Reports Medicine

Article Title: HE4 drives PD-L1 expression in myeloid cells via IFN-γR-JAK-STAT3 signaling to promote tumor immune evasion

doi: 10.1016/j.xcrm.2026.102691

Figure Lengend Snippet: HE4 neutralization exerts therapeutic activity in human cancer models (A–C) PMA-differentiated THP-1 macrophages were stimulated with Fc or hHE4-Fc, and PD-L1 expression was assessed by flow cytometry (A), immunoblotting (B), and RT-qPCR (C); a commercial hHE4-Fc was included as an independent control. (D) Binding of hHE4 to PMA-differentiated THP-1 cells assessed by flow cytometry. (E and F) PMA-differentiated THP-1 cells were pretreated with ruxolitinib, fludarabine, or Stattic, followed by hHE4-Fc stimulation; PD-L1 was quantified by RT-qPCR (E) and flow cytometry (F). (G and H) Anti-hHE4 monoclonal antibodies inhibited hHE4-induced PD-L1 upregulation in PMA-differentiated THP-1 cells, assessed by RT-qPCR (G) and flow cytometry (H). (I) Anti-hHE4 mAb clone #10 blocked hHE4 binding to PMA-differentiated THP-1 cells. (J) Binding of wild-type or epitope-mutant hHE4-Fc to anti-hHE4 mAb clone #10 was quantified by ELISA. (K) Pharmacokinetic analysis of anti-hHE4 mAb clone #10 in C57BL/6 mice following intravenous administration. (L–O) Fresh human LUAD tumor cell suspensions were treated with anti-hHE4 mAb clone #10, followed by flow cytometric analysis of PD-L1 and ELISA measurement of IFN-γ and granzyme B. (P) Recombinant HE4 suppressed IFN-γ production in human LUAD tumor cell suspensions. (Q–T) HE4 blockade enhanced PBMC-mediated antitumor activity in humanized C-NKG mice bearing OVCAR3 or NCI-H358 tumors, shown by treatment scheme, representative tumors, and tumor weights. Schematics (L and Q) were created using BioRender. Statistical analyses were performed using one-way ANOVA (C, E, and G), paired t tests (M–P), or unpaired t tests (S and T). Data in (A–J) are representative of three independent experiments; data in (Q–T) are pooled from two independent experiments.

Article Snippet: Human: OVCAR3 , ATCC , Cat# HTB161.

Techniques: Neutralization, Activity Assay, Expressing, Flow Cytometry, Western Blot, Quantitative RT-PCR, Control, Binding Assay, Bioprocessing, Mutagenesis, Enzyme-linked Immunosorbent Assay, Recombinant