The KDM5B Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian carcinoma cell line A2780. This loss-of-function model was generated by CRISPR/Cas9-mediated disruption of the KDM5B gene, producing a heterogeneous pool of cells with targeted gene inactivation that preserves the natural diversity of editing outcomes.
The A2780 cell line is an epithelial ovarian cancer model established from an untreated patient, retaining wild-type p53. These cells are widely used for studying ovarian cancer biology, drug resistance, and epigenetic regulation, providing a clinically relevant and consistent background for knockout experiments.
KDM5B encodes a histone H3K4 demethylase that removes methyl groups from H3K4me3 and H3K4me2, repressing transcription of target genes. KDM5B is transcriptionally activated by MYC and responsive to retinoic acid, hypoxia, and PI3K/AKT signaling. It interacts with HDAC1/2, EZH2, SUZ12, and RbBP5 to coordinate chromatin silencing. Its demethylase activity represses downstream targets including HOX genes, CDKN1A, CCND1, and stemness factors NANOG and SOX2, linking chromatin modification to control of proliferation and differentiation.
In A2780 cells, KDM5B knockout derepresses tumor suppressors and differentiation factors, reducing proliferation and increasing sensitivity to agents like cisplatin. The polyclonal population enables investigation of KDM5B??s role in oncogenic maintenance, drug resistance, and stemness, without clonal bias. The wild-type p53 background allows studies on KDM5B-p53 interplay.
These knockout cells support applications in ovarian cancer epigenetics, including drug sensitivity assays, cancer stem cell studies, and tumor suppressor reactivation. Representative techniques include western blotting, RT-qPCR, ChIP-qPCR for H3K4me3, RNA-seq, MTS proliferation assays, colony formation, flow cytometry, and cisplatin sensitivity testing. For further information, please contact Ascent Research.
