The CCDC88C Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the gene encoding CCDC88C (Daple), a scaffold protein that integrates Wnt signaling pathways. This mixed population of HeLa cells contains a spectrum of editing events at the CCDC88C locus, yielding heterogeneous loss of CCDC88C function and serving as a versatile tool for studying the consequences of CCDC88C ablation without single-cell clonal selection. The product enables investigation of both canonical and non-canonical Wnt pathway dynamics in a widely used human epithelial cancer model.
The host HeLa cell line is an immortalized human cervical adenocarcinoma epithelial line originally derived from an HPV18-positive tumor. HeLa cells exhibit aneuploidy and robust proliferative capacity, making them a standard model for cancer biology, drug screening, and gene function studies. Their endogenous expression of Wnt pathway components and responsiveness to Wnt ligands make them suitable for dissecting CCDC88C-mediated signaling, although users should account for the inherent genomic instability characteristic of this cell line.
CCDC88C functions as a negative regulator of canonical Wnt/??-catenin signaling by binding Dishevelled (DVL) proteins and preventing ??-catenin nuclear translocation, thereby suppressing transcription of targets such as MYC and CCND1. Simultaneously, it acts as a positive regulator of non-canonical Wnt/planar cell polarity (PCP) signaling, coupling Frizzled receptor activation by Wnt5a or Wnt11 to downstream effectors including RhoA, Rac1, and JNK. Additionally, CCDC88C participates in ciliogenesis through interactions with DVL and Rho GTPases. Consequently, CCDC88C knockout leads to enhanced ??-catenin transcriptional activity, increased expression of proliferative genes, and impaired PCP-dependent processes and cilia formation.
In the HeLa context, CCDC88C disruption is predicted to elevate constitutive ??-catenin signaling due to the loss of DVL sequestration, potentially driving upregulation of MYC and CCND1 and promoting cell proliferation and survival. Concurrently, defective RhoA and Rac1 activation may alter actin cytoskeleton dynamics, cell migration, and planar polarity. The loss of ciliogenesis-related functions could further affect cellular signaling compartments. These changes make the CCDC88C knockout HeLa polyclonal cells a relevant model for examining how dysregulated Wnt pathway crosstalk contributes to malignant phenotypes in cervical adenocarcinoma and other cancers.
Researchers can employ these polyclonal cells in diverse applications including dissection of Wnt signaling mechanisms, cancer cell proliferation and migration assays, planar cell polarity research, and ciliogenesis analysis. Representative assays include TOP/FOP luciferase reporter assays to measure ??-catenin transcriptional activity, western blotting for CCDC88C and downstream targets (??-catenin, MYC, CCND1), RhoA/Rac1 activation pull-downs, scratch wound and Transwell migration/invasion assays, immunofluorescence localization of ??-catenin and ciliary markers (ARL13B, IFT88), and JNK phosphorylation analysis. The polyclonal nature enables study of heterogeneous knockout effects, providing a more physiologically relevant population-level readout. For additional product information, please contact Ascent Research.
