The CCPG1 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1299 human non-small cell lung carcinoma line. This product achieves disruption of the CCPG1 gene, which encodes a critical positive regulator of the G2/M transition. By abrogating CCPG1 function, researchers gain a loss-of-function model to interrogate mitotic progression, cell cycle regulation, and cancer cell vulnerabilities in a defined genetic background.
The NCI-H1299 parental cell line originates from a metastatic lymph node of a non-small cell lung carcinoma patient. It displays epithelial morphology and harbors a homozygous deletion of the TP53 tumor suppressor gene, conferring a mesenchymal phenotype. Widely employed as a model for NSCLC, this p53-null background disrupts the G1/S checkpoint and heightens dependence on the G2/M checkpoint, making it ideal for studying cell cycle control and chromosomal instability.
CCPG1 directly binds and activates the cyclin B1-CDK1 complex, thereby driving mitotic entry. Its expression is regulated by the transcription factors E2F1 and FOXM1, and it interacts with CCNB1, CDK1, and PLK1 to orchestrate mitotic events. Within the broader signaling network, CCPG1 functions alongside PLK1, Aurora A, and BUBR1, linking it to the spindle assembly checkpoint and the anaphase promoting complex/cyclosome (APC/C). Thus, CCPG1 serves as a key node integrating cell cycle transcriptional outputs with mitotic execution.
In the TP53-deficient NCI-H1299 context, loss of CCPG1 leads to mitotic arrest and diminished proliferation, underscoring the reliance of these cells on G2/M checkpoint integrity. This polyclonal knockout population enables dissection of synthetic lethal relationships, investigation of chromosomal instability pathways, and assessment of sensitivity to antimitotic drugs. It provides a physiologically relevant platform for exploring how cancer cells with compromised checkpoints adapt to defects in mitotic regulation.
Key experimental applications include flow cytometry with propidium iodide for cell cycle distribution, Western blotting for cyclin B1 and phospho-histone H3, immunofluorescence staining of ??-tubulin and pericentrin to visualize spindle morphology, and RT-qPCR analysis of mitotic gene expression. Additionally, these cells are suitable for colony formation assays, Annexin V apoptosis studies, and live-cell imaging to track mitotic progression. For further technical specifications or to place an order, please contact Ascent Research.
