The CCN1 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HeLa cell line. This product provides a heterogeneous pool of cells carrying targeted disruption of the CCN1 gene, enabling loss-of-function studies without clonal selection. The polyclonal format preserves genetic diversity and minimizes clonal artifacts, making it suitable for experiments where phenotypic consistency across a population is desired. The CRISPR/Cas9-mediated gene disruption offers a robust model for investigating CCN1-dependent cellular processes in a widely used cervical adenocarcinoma background.
The HeLa cell line is an established model originated from a HPV-18-positive cervical carcinoma and represents transformed epithelial cells with unlimited proliferative capacity. These cells are extensively characterized and serve as a standard platform for cancer biology, epithelial cell research, and drug screening. The HeLa background provides a well-defined genetic and epigenetic landscape that facilitates the interpretation of gene knockout effects, particularly in studies of adhesion, migration, and signal transduction.
CCN1 (also known as CYR61) is a matricellular protein that bridges cell-surface integrins with extracellular matrix components, regulating fundamental cellular behaviors. Upon secretion, CCN1 binds integrin receptors such as ??v??3, ??v??5, and ??6??1, initiating intracellular signaling cascades including FAK/Src activation, which subsequently stimulates PI3K/Akt and Ras/MAPK pathways. These pathways converge to promote cell adhesion, migration, proliferation, and survival. CCN1 also modulates Wnt and TGF-?? signaling and is itself transcriptionally upregulated by TGF-??, FGF, PDGF, and hypoxia via AP-1, NF-??B, and HIF-1??. Downstream, CCN1 enhances expression of pro-angiogenic factors like VEGF and matrix metalloproteinases MMP-2 and MMP-9, while also upregulating COX-2 and anti-apoptotic Bcl-2.
In the HeLa cervical adenocarcinoma model, knockout of CCN1 is expected to impair cell-ECM interactions and attenuate integrin-dependent signaling pathways critical for tumor cell behavior. Given CCN1??s role in promoting migration, invasion, and angiogenesis, this polyclonal knockout pool provides a physiologically relevant system to dissect its contributions to cancer progression. The absence of CCN1 may reduce activation of FAK and Akt, leading to decreased motility and survival, which can be exploited to study metastatic mechanisms or to evaluate therapeutic vulnerabilities in epithelial tumors.
This polyclonal CCN1 knockout cell product is ideally suited for a range of experimental applications including wound healing and transwell invasion assays to assess migration, apoptosis flow cytometry to measure cell death, phospho-signaling analysis to probe kinase activation, and cell adhesion assays to interrogate matrix attachment. It also enables drug sensitivity screening and dissection of CCN1-dependent signaling networks via western blotting, RT-qPCR, and immunofluorescence. For further information or to discuss custom genome engineering projects, please contact Ascent Research.
