The BAP1 Knockout LoVo Polyclonal Cells constitute a genetically engineered human colorectal adenocarcinoma cell population in which the BAP1 tumor suppressor gene has been disrupted through CRISPR/Cas9-mediated gene editing. This polyclonal knockout cell pool provides a loss-of-function model that enables robust investigation of BAP1-dependent cellular processes without the clonal selection biases associated with monoclonal lines. The heterogeneous nature of the polyclonal population captures a range of editing outcomes, offering a physiologically relevant system for studying BAP1 deficiency in a colorectal cancer context.
Derived from a metastatic lymph node of a patient with colon adenocarcinoma, the LoVo host cell line is a well-established epithelial model widely employed in colorectal cancer research. LoVo cells exhibit key characteristics of colorectal adenocarcinoma, including aberrant Wnt signaling and microsatellite instability, making them a suitable platform for examining the molecular underpinnings of colorectal tumorigenesis. Their adherent growth and robust proliferation facilitate a broad spectrum of downstream assays, from biochemical analyses to functional genomic screens.
BAP1 encodes a deubiquitinating enzyme that functions within the PR?DUB complex alongside ASXL1, ASXL2, and HCFC1 to remove monoubiquitin from histone H2A at lysine 119 (H2AK119ub). This activity promotes chromatin accessibility and transcriptional regulation. BAP1 acts downstream of DNA damage sensors such as ATM and ATR kinases, and it interacts directly with BRCA1 to coordinate DNA repair. Among its downstream targets, BAP1-mediated deubiquitination influences the INO80 chromatin remodeling complex, modulates expression of the cyclin?dependent kinase inhibitor p21 (CDKN1A), and governs the pro?apoptotic factor BAX. Through these interactions, BAP1 maintains genomic stability by coupling chromatin dynamics to cell cycle arrest and apoptosis in response to genotoxic stress.
In the LoVo colorectal adenocarcinoma background, BAP1 disruption profoundly perturbs these tumor suppressive pathways. Loss of BAP1 deubiquitinase activity is expected to elevate H2AK119ub levels, leading to aberrant gene silencing and compromised DNA damage repair. This creates a vulnerable cellular state that recapitulates aspects of BAP1-mutant colorectal cancers, where defective chromatin regulation and impaired apoptosis contribute to oncogenic progression and therapeutic resistance. The knockout model thus serves as a critical tool for dissecting the role of BAP1 in colorectal tumor biology and for exploring synthetic lethal interactions or drug sensitivities.
These polyclonal knockout cells are ideally suited for a variety of advanced research applications. Investigators can employ Western blotting to confirm BAP1 protein loss and assess changes in H2AK119ub levels, or use ChIP?qPCR to map histone modification landscapes at specific loci. Immunofluorescence detection of ??H2AX foci provides a readout of DNA double?strand break accumulation, while Annexin V assays and cell viability measurements enable quantitative analysis of apoptosis and drug response. Furthermore, the cells can be challenged with chemotherapeutics such as cisplatin in drug sensitivity testing, or evaluated by Comet assay for DNA damage. All these applications empower detailed functional genomics studies, tumor suppressor analyses, and drug resistance investigations. For additional product details or custom requests, please contact Ascent Research.
