The CCDC116 Knockout HeLa Polyclonal Cells product represents a CRISPR/Cas9-mediated gene disruption model in which the endogenous CCDC116 locus has been targeted to create a polyclonal knockout population. This pool of edited HeLa cells carries heterogeneous loss-of-function mutations at the target site, generating a versatile tool for studying CCDC116-dependent phenotypes. The polyclonal format avoids clonal selection artifacts and provides a broadly representative model for functional investigations. The knockout cells are suitable for diverse experimental applications including signaling studies, phenotypic screens, and drug discovery.
HeLa is an immortalized human cervical adenocarcinoma cell line established from a cervical carcinoma biopsy. This widely employed model is HPV18-positive, aneuploid, and exhibits robust proliferative capacity. HeLa cells are a cornerstone of molecular and cell biology research, having contributed to seminal discoveries in cell cycle regulation, signal transduction, and cancer biology. Their well-characterized genomic landscape and ease of culture make them an ideal host for loss-of-function studies. The cervical cancer origin provides a physiologically relevant background for exploring pathways dysregulated in epithelial tumors, including those governing epithelial-mesenchymal transition and metastatic progression.
CCDC116 encodes a coiled-coil domain-containing protein that promotes cell proliferation, migration, and cancer stemness. Mechanistically, CCDC116 physically interacts with the transcription factor SNAI1 to suppress E-cadherin expression, thereby driving epithelial-mesenchymal transition. In parallel, CCDC116 enhances Wnt/??-catenin signaling, leading to increased transcriptional activity of ??-catenin/TCF complexes and upregulation of pro-proliferative target genes such as MYC and CCND1. The protein likely functions downstream of upstream Wnt signals, although direct upstream regulators remain poorly defined. Representative pathway components include ??-catenin, TCF4, SNAI1, E-cadherin, vimentin, GSK3??, AXIN, and Wnt ligands. Cooperation between the EMT and Wnt programs underscores the multifaceted role of CCDC116 in oncogenic signaling.
In the HeLa cell context, disruption of CCDC116 is anticipated to attenuate Wnt/??-catenin pathway activity and impair EMT-associated phenotypes, providing a functional readout for target engagement. Given HeLa??s aneuploidy and HPV-driven transformation, this knockout model enables dissection of CCDC116??s contribution to pathways frequently co-opted in cervical and other epithelial cancers. Researchers can assess how loss of CCDC116 alters ??-catenin subcellular localization, SNAI1-mediated transcriptional repression, and the expression of EMT markers such as E-cadherin and vimentin. The model thus offers a platform to interrogate the interplay between viral oncoproteins, genomic instability, and CCDC116-dependent signaling circuits.
This polyclonal knockout cell population supports a broad range of research applications. It can be employed in western blotting for EMT markers, wound healing assays, Transwell migration and invasion experiments, and MTT proliferation assays to quantify metastatic and growth phenotypes. Immunofluorescence can detect ??-catenin localization changes, while TOP/FOP luciferase reporter assays measure Wnt pathway activity. Co-immunoprecipitation studies can confirm the CCDC116-SNAI1 interaction. Beyond functional characterization, the cells are suitable for drug target validation and anti-cancer compound screening in Wnt- or EMT-focused campaigns. For further technical details or ordering information, please contact Ascent Research.
