The CCDC102B Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited human cell population engineered for targeted disruption of the CCDC102B gene within the HeLa cervical adenocarcinoma line. This polyclonal knockout pool provides a heterogeneous loss-of-function model that avoids clonal bias, enabling robust analysis of CCDC102B functional roles. The product is supplied as a ready-to-use frozen vial, suitable for immediate expansion in standard culture conditions, and serves as a critical tool for dissecting Wnt/??-catenin signaling regulation in cancer research.
Derived from the HPV18-positive HeLa cell line, these cells retain the molecular characteristics of an aggressive cervical carcinoma, including aberrant activation of signaling pathways that drive uncontrolled proliferation. HeLa cells are a foundational model in cancer biology, widely employed to study oncogenic mechanisms, tumor suppressor networks, and therapeutic responses. Their established use in signal transduction research, particularly the Wnt pathway, makes them an ideal host for knockout studies of negative regulators such as CCDC102B.
The CCDC102B gene encodes a coiled-coil domain protein that negatively regulates canonical Wnt/??-catenin signaling by promoting degradation of ??-catenin (CTNNB1). It interacts with GSK3B and APC within the destruction complex to facilitate ??-catenin phosphorylation and turnover. DNA methylation regulates CCDC102B expression. Knockout disrupts this negative control, stabilizing ??-catenin, which then translocates to the nucleus, activates TCF/LEF transcription factors, and upregulates targets including CCND1, MYC, LEF1, and AXIN2. The pathway involves WNT ligands, FZD receptors, LRP5/6, and DVL.
In the HeLa cell context, where basal Wnt activity contributes to the transformed phenotype, CCDC102B knockout further amplifies pathway output, creating a sensitized model to dissect the consequences of unleashed Wnt signaling. The resulting enhanced expression of proliferative and migratory genes mirrors oncogenic progression observed in cervical, breast, and other solid tumors. This model thus enables investigation of how loss of a putative tumor suppressor exacerbates malignant traits, providing a physiologically relevant platform to explore Wnt-dependent mechanisms of tumorigenesis and metastasis.
Researchers can employ these cells in diverse applications, including mechanistic studies of Wnt/??-catenin signal transduction, functional dissection of the destruction complex, and evaluation of candidate Wnt inhibitors in drug screening campaigns. Compatible assays include quantitative western blotting to monitor ??-catenin and target protein levels, TOPFlash/FOPFlash dual-luciferase reporter assays to measure TCF/LEF transcriptional activity, RT-qPCR for Wnt-responsive genes, and immunofluorescence for ??-catenin subcellular localization. Cell proliferation and migration assays further extend the utility of this model to phenotypic analyses. For further details on product validation, protocols, or troubleshooting, please contact Ascent Research.
