The CCDC117 Knockout NCI-H1975 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human NCI-H1975 non-small cell lung adenocarcinoma cell line. This product provides a genetically heterogeneous loss-of-function model for the coiled-coil domain-containing protein 117 (CCDC117), enabling investigation of its role in mitotic progression without relying on a single clonal isolate. The polyclonal format captures a range of editing events across the cell population, offering a robust system for studying gene disruption effects in cancer cell biology.
The parental NCI-H1975 cell line is an epithelial cancer model isolated from a lung adenocarcinoma patient, harboring endogenous EGFR L858R and T790M mutations. These mutations confer sensitivity to first- and third-generation EGFR tyrosine kinase inhibitors while the T790M gatekeeper mutation is a primary driver of acquired resistance. Consequently, NCI-H1975 is a widely employed model for investigating EGFR-targeted therapy resistance, tumor cell proliferation, and associated signaling networks.
CCDC117 encodes a coiled-coil domain protein that acts as a critical regulator of mitotic progression. It is phosphorylated by the Polo-like kinase 1 (PLK1), a master mitotic kinase, and this phosphorylation event is essential for proper chromosome alignment and segregation. CCDC117 interacts directly with PLK1 and associates with microtubule-associated proteins and kinetochore components, functioning within the PLK1 signaling axis. Representative pathway components include PLK1, CCDC117, kinetochore proteins, and Aurora kinases, placing CCDC117 at the interface of mitotic spindle assembly and chromosome dynamics.
In the context of NCI-H1975 cells, disruption of CCDC117 provides a unique tool to dissect how mitotic regulatory networks intersect with oncogenic signaling driven by mutant EGFR. Since chromosomal instability is a hallmark of many solid tumors, including lung adenocarcinoma, CCDC117 knockout can be used to examine the consequences of impaired mitotic fidelity on cancer cell viability, proliferation, and therapeutic response. This model may be particularly informative for studying synthetic lethal interactions or enhanced sensitivity to mitotic inhibitors in cells already compromised by EGFR-driven proliferation.
Typical applications for these polyclonal knockout cells include detailed cell cycle analysis by flow cytometry, immunofluorescence visualization of mitotic spindle abnormalities, and time-lapse microscopy to track mitotic progression defects. Researchers can validate loss of CCDC117 function by western blotting for phospho-CCDC117 or total protein levels, and assess functional consequences through proliferation and clonogenic survival assays. This polyclonal knockout population is also suitable for investigating PLK1-related signaling dynamics and chromosomal instability in a genetically relevant lung cancer background. For additional product specifications and technical support, please contact Ascent Research.
