The CCDC85C Knockout HT29 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of HT29 colorectal adenocarcinoma cells with disrupted CCDC85C. This heterogeneous knockout pool enables robust loss-of-function studies while avoiding clonal selection biases. The polyclonal format is ideal for functional screens and population-level analyses.
HT29 cells were derived from a colorectal adenocarcinoma of a 44-year-old female Caucasian patient. As adherent epithelial cells with aberrant Wnt signaling due to APC mutation, they serve as a standard model for colon cancer biology, tumor progression, and drug response investigations.
CCDC85C encodes a coiled-coil domain protein implicated in protein?Cprotein interactions potentially linking the cytoskeleton to cell cycle control. It is hypothesized to interact with cytoskeletal proteins like ??-actin (ACTB) and ??-tubulin (TUBB) and may be modulated by or converge on pathways involving cyclin-dependent kinase 1 (CDK1) and ??-catenin (CTNNB1). Context-dependent Wnt pathway involvement further suggests that CCDC85C could influence CTNNB1 transcriptional programs, with knockout expected to perturb cytoskeletal dynamics and cell cycle progression.
In HT29 cells, CCDC85C knockout is anticipated to alter proliferation, migration, and Wnt responsiveness, directly impacting colorectal cancer phenotypes. Disruption of CCDC85C function may impair migratory capacity, reduce growth, or promote apoptosis, offering a model to dissect coiled-coil domain protein contributions to colon tumorigenesis and drug sensitivity.
This knockout model supports diverse assays such as Western blotting and RT-qPCR for target disruption verification, proliferation assays (MTT, BrdU, colony formation), Transwell migration/invasion, flow cytometry for cell cycle and apoptosis, and immunofluorescence for cytoskeletal markers. High-content approaches including RNA-seq and phospho-signaling profiling enable in-depth mechanistic studies. Applications span functional characterization, signaling dissection, and drug target validation in colorectal cancer. Please contact Ascent Research for further technical details.
