The CCPG1 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric cancer cell line, featuring targeted disruption of the CCPG1 gene. This polyclonal knockout model provides a heterogenous pool of cells carrying distinct loss-of-function alleles of CCPG1, enabling robust investigation of gene function without the clonal selection biases inherent in monoclonal lines. The product is supplied as a ready-to-use population of proliferating polyclonal knockout cells, validated for genomic CCPG1 disruption and suited for downstream functional assays. Researchers can employ this model to dissect the role of CCPG1 in cell cycle control and gastric cancer biology.
The HGC-27 parental cell line was established from the metastatic lymph node of a patient with gastric carcinoma and displays an epithelial morphology characteristic of advanced gastric cancer. This cell line is widely used as a model system for studying the molecular mechanisms driving gastric cancer metastasis and progression. HGC-27 cells harbor genetic alterations common in gastric malignancies, making them particularly relevant for investigating oncogenic signaling and tumor cell proliferation. The epithelial phenotype and metastatic origin of HGC-27 render this host cell background valuable for translational research aimed at understanding gastric cancer dissemination.
CCPG1 functions as a cell cycle regulator that promotes the G1/S transition through the E2F signaling pathway. Acting downstream of E2F1 and mitogenic growth signals, CCPG1 facilitates transcriptional activation of cyclins CCND1 and CCNE1. It interacts with the pocket protein RB1 and E2F family members E2F4 and E2F5 to form regulatory complexes. Downstream effectors include CDK2 and CDK4, which drive cycle progression. CCPG1 knockout impairs E2F-mediated cyclin induction, attenuating CDK activity and causing cell cycle arrest.
In the context of HGC-27 gastric cancer cells, CCPG1 knockout provides a powerful tool to evaluate the dependence of metastatic gastric carcinoma on CCPG1-driven proliferation. As HGC-27 cells originate from a metastatic site, this model is particularly suited for dissecting the contributions of cell cycle dysregulation to gastric cancer progression and metastasis. The loss of CCPG1 is expected to reduce the expression of G1/S cyclins and inhibit E2F target gene activation, leading to diminished proliferative capacity. This cellular background thus enables researchers to study the interplay between CCPG1 and other signaling networks that sustain gastric tumor growth in a clinically relevant setting.
This CCPG1 knockout product enables studies of cell cycle regulation, gastric cancer pathogenesis, and anticancer drug target validation. Typical applications include flow cytometry for cell cycle distribution, western blotting for cyclins D1/E1 and CDK2/4, and RT-qPCR for E2F target genes. Proliferation assays such as colony formation, MTS/MTT, and EdU incorporation are also applicable. The polyclonal knockout format provides a population-level view of CCPG1 loss-of-function effects. For additional information, please contact Ascent Research.
