The CBX5 Knockout 143B Polyclonal Cells product from Ascent Research provides a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the CBX5 gene in the human 143B osteosarcoma cell line. This loss-of-function model is generated by CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous polyclonal pool that facilitates robust downstream analyses.
The 143B cell line is a well-characterized human osteosarcoma model that harbors a TP53 mutation, rendering it p53-deficient and highly tumorigenic with pronounced metastatic capability. These adherent cells are widely utilized in bone cancer research, particularly for investigating drug resistance mechanisms and tumor aggressiveness in a genetic background lacking functional p53 tumor suppressor activity.
CBX5 encodes heterochromatin protein 1?? (HP1??), a key reader of histone H3 lysine 9 trimethylation (H3K9me3) marks deposited primarily by SUV39H1/2 and SETDB1 methyltransferases. HP1?? interacts with cofactors including TRIM28 (KAP1), LBR, DNMT1, and the retinoblastoma protein (pRb) to establish compact heterochromatin, repress E2F target genes such as cyclin E1, and silence centromeric repeats and retrotransposons. Upstream, its recruitment is regulated by DNA damage kinases ATM and ATR, linking heterochromatin integrity to genomic surveillance. Disruption of CBX5 leads to heterochromatin decompaction, derepression of E2F-driven transcription, aberrant centromere function, and retrotransposon activation, culminating in heightened genomic instability.
In the 143B background, loss of CBX5 synergizes with p53 deficiency to exacerbate genomic instability, potentially affecting cell cycle regulation, senescence bypass, and metastatic behavior. This polyclonal knockout model enables dissection of HP1???Cdependent tumor-suppressive and oncogenic mechanisms in a highly aggressive osteosarcoma context, shedding light on how epigenetic dysregulation contributes to cancer progression and therapy resistance.
Researchers can leverage this polyclonal knockout cell population for chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) of H3K9me3 and CBX5 occupancy, immunofluorescence visualization of heterochromatin foci disruption, western blot confirmation of HP1?? loss, and RT-qPCR profiling of downstream targets such as CDKN1A and E2F1. Functional assays including flow cytometric cell cycle analysis, colony formation, wound healing migration, and senescence-associated ??-galactosidase staining can link heterochromatin defects to phenotypic outcomes. This product is ideally suited for heterochromatin biology, epigenetic drug target validation, osteosarcoma metastasis research, and mechanistic studies of the SUV39H1/2?CCBX5?CTRIM28 axis. For additional information or customization, please contact Ascent Research.
