The CBX2 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-mediated gene-disrupted population targeting the CBX2 gene in the HeLa cell line. This polyclonal knockout format yields a heterogeneous pool of edited cells that enables functional study of CBX2-dependent processes without clonal artifacts, offering a robust loss-of-function model for population-based assays.
HeLa cells are an immortalized epithelial line isolated from a cervical adenocarcinoma containing integrated HPV18 DNA. Widely used in biomedical research, they have a stable pseudodiploid karyotype and exhibit aggressive growth in vitro, making them a standard host for studying oncogenic signaling, epigenetic mechanisms, and therapeutic responses.
CBX2 is a chromodomain-containing subunit of Polycomb repressive complex 1 (PRC1). It recognizes H3K27me3 marks deposited by PRC2 (comprising EZH2, SUZ12, and EED) and, together with RING1B and BMI1, catalyzes H2AK119 monoubiquitination, leading to chromatin compaction. CBX2 interacts with PHC1?C3 and other CBX family members to maintain silencing of target loci. Under upstream developmental cues and PRC2 activity, CBX2-mediated repression influences key downstream genes such as Hox clusters, CDKN2A, and p53 transcriptional targets, thereby controlling differentiation, proliferation, and tumor suppression.
In the context of HeLa cervical adenocarcinoma cells, CBX2 knockout permits dissection of Polycomb-dependent gene silencing pathways that are dysregulated in cancer. Given CBX2??s involvement in breast, prostate, ovarian, and glioblastoma malignancies, this model supports investigations into how PRC1 activity modulates chromatin states and oncogenic phenotypes in a HPV-positive background.
Researchers can employ this population in ChIP-qPCR to analyze histone modifications, RNA-seq for transcriptomic profiling, Western blotting for PRC1 complex integrity, and ATAC-seq to assess chromatin accessibility. Proliferation, colony formation, and flow cytometry assays further enable functional characterization of CBX2 loss. The model is applicable to epigenetic regulation, cancer biology, and developmental research requiring population-level readouts. For further details, please contact Ascent Research.
