The CCDC85C Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line, engineered to disrupt the CCDC85C gene. This product provides a heterogeneous pool of cells with targeted gene disruption, creating a loss-of-function model that preserves genetic diversity while eliminating CCDC85C expression. The polyclonal format minimizes clonal selection biases and offers a reliable tool for studying CCDC85C function in centriolar satellite biology, ciliogenesis, and related signaling pathways.
HeLa cells are a widely utilized epithelial cell line originally isolated from a cervical adenocarcinoma, serving as a foundational model in cancer research, virology, and cell biology. Their robust growth characteristics and established genetic manipulation protocols make them an ideal host for generating knockout models. In this context, CCDC85C disruption in HeLa cells provides a unique platform to examine the role of centriolar satellites in cancer cell behavior and ciliary signaling.
CCDC85C is a core component of centriolar satellites, granular structures that cluster around the centrosome and regulate microtubule organization, cilia assembly, and protein trafficking. It interacts with key satellite proteins such as PCM1, CEP290, and CEP131, forming complexes that facilitate satellite biogenesis and ciliary vesicle transport. CCDC85C functions downstream of putative transcriptional regulators like RFX3 and FOXJ1, which are known to drive ciliogenic gene expression. Although its direct downstream targets remain undefined, CCDC85C likely influences ciliary membrane formation and Hedgehog pathway activation. Disruption of CCDC85C is expected to impair primary cilium assembly, thereby attenuating Hedgehog signaling??a pathway mediated by SMO and GLI transcription factors that governs cell fate and proliferation.
In the HeLa adenocarcinoma background, CCDC85C knockout holds particular significance for cancer biology. Primary cilia are frequently lost or disassembled in malignant cells, and their absence correlates with aberrant Hedgehog signaling and uncontrolled proliferation. By ablating CCDC85C, this model enables dissection of the relationship between centriolar satellite integrity, ciliogenesis, and oncogenic processes. Researchers can explore how ciliary dysfunction alters cell cycle progression, migration, and invasion in a well-characterized cervical cancer context, potentially uncovering novel therapeutic vulnerabilities.
This polyclonal knockout cell population is suitable for diverse experimental applications. It can be employed to investigate mechanisms of ciliogenesis using immunofluorescence microscopy to detect ciliary markers (e.g., acetylated ??-tubulin), or to assess signaling changes by RT-qPCR analysis of Hedgehog target genes (e.g., GLI1, PTCH1). Western blotting for ciliary components like ARL13B and IFT88 validates protein-level alterations, while flow cytometry enables cell cycle profiling. Altered migratory and invasive capacities can be examined via Transwell assays. The model also supports drug screening campaigns targeting cilia-dependent pathways or ciliopathies. For further information, please contact Ascent Research.
