The CCDC14 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population for studying coiled-coil domain-containing protein 14 (CCDC14) in a cervical cancer background. These HeLa cells carry targeted gene disruption, creating a loss-of-function model to explore CCDC14??s functions in ciliogenesis, centrosome biology, and related signaling. The polyclonal nature retains genetic diversity from editing, enabling unbiased phenotypic assessment.
The host cell line, HeLa, is a classic human cervical adenocarcinoma line positive for human papillomavirus type 18 (HPV-18). These epithelial cells are widely used in cancer research due to their aggressive growth, well-characterized genome, and capacity to form primary cilia under serum-starvation conditions. The HPV-18 E6 and E7 oncoproteins disrupt p53 and retinoblastoma protein functions, contributing to genomic instability and altered cell cycle regulation, which makes HeLa cells particularly useful for studying the intersection of oncogenic signaling and ciliary biology.
CCDC14 encodes a coiled-coil domain-containing protein that localizes to centrosomes and basal bodies, where it promotes centriole cohesion and microtubule anchoring, processes essential for primary cilium assembly. It directly interacts with centrosomal proteins CEP63 and CEP152, and its disruption impairs ciliogenesis, leading to defective Hedgehog signal transduction. Specifically, CCDC14 knockout attenuates activation of the transmembrane protein SMO, resulting in decreased transcription of downstream effectors including GLI1 and PTCH1. Moreover, CCDC14 loss disrupts microtubule organization and may intersect with Wnt/??-catenin signaling, linking it to broader cellular processes such as cell cycle progression and cytoskeletal dynamics.
In the HeLa cell context, CCDC14 disruption provides a powerful platform to examine how ciliary defects influence cervical cancer cell behavior. Given the emerging roles of primary cilia in cancer??including regulation of proliferation, migration, and drug resistance??this knockout model allows dissection of CCDC14??s contributions to these processes. Because HeLa cells harbor HPV-18 oncoproteins that manipulate cell cycle checkpoints, the combined effect of CCDC14 loss may reveal synergistic impacts on genomic stability, Hedgehog-dependent growth, and invasive potential, offering insights into ciliopathy-associated cancer mechanisms.
Researchers can employ these CCDC14 Knockout HeLa Polyclonal Cells for a variety of applications, including mechanistic studies of ciliogenesis using immunofluorescence detection of ciliary markers such as acetylated ??-tubulin and Arl13b, analysis of Hedgehog signaling via RT-qPCR for GLI1 and PTCH1, and assessment of cell cycle alterations through flow cytometry. Western blotting for CCDC14 and associated centrosomal proteins, as well as migration and invasion experiments, can be conducted to evaluate metastatic phenotypes. Phospho-signaling analyses can further elucidate kinase pathways regulated by CCDC14. For further information or technical support regarding this product, please contact Ascent Research.
