The CCSER1 Knockout NCI-H1975 Polyclonal Cells product comprises a CRISPR/Cas9-mediated polyclonal knockout cell population targeting the human CCSER1 gene in the NCI-H1975 lung adenocarcinoma cell line. This product is supplied as a population of edited cells, providing a heterogeneous knockout model suitable for studying loss-of-function effects without clonal isolation. The polyclonal format retains biological variability while enabling robust functional genomics investigations of CCSER1 in a disease-relevant background.
The host NCI-H1975 cell line is derived from a human non-small cell lung cancer (NSCLC) adenocarcinoma with an endogenous EGFR L858R activating mutation, a common driver alteration in lung oncology. This well-characterized model exhibits hallmark features of NSCLC, including dysregulated proliferation and sensitivity to EGFR-targeted therapies. The L858R mutation renders the cells dependent on oncogenic EGFR signaling, making them a valuable platform for exploring tumor suppressor genes like CCSER1 within the context of aberrant growth factor pathways.
CCSER1 encodes a coiled-coil serine-rich protein that functions as a key regulator of cytokinesis and microtubule dynamics. The protein directly interacts with ??-tubulin and ??-tubulin to modulate microtubule stability and organization during cell division. CCSER1 operates within a signaling node that includes Aurora kinase B and the RhoGEF ECT2, both critical for central spindle formation and cleavage furrow ingression. Mechanistically, CCSER1 participates in the spatiotemporal control of cytokinesis by influencing microtubule behavior, thereby ensuring proper chromosome segregation and abscission. Loss of CCSER1 disrupts these processes, leading to cytokinetic failure, multinucleation, and genomic instability??hallmarks of tumorigenesis.
In the NCI-H1975 context, CCSER1 deletion generates a physiologically relevant model to dissect its putative tumor suppressor role in NSCLC. The EGFR L858R-driven background cooperates with defective cytokinesis to accelerate malignant phenotypes, including enhanced proliferation, aneuploidy, and invasive capacity. This model enables dissection of CCSER1-dependent mechanisms that restrain tumor progression, particularly how microtubule dysregulation contributes to chromosomal instability in lung adenocarcinoma. By combining the NCI-H1975 genetic landscape with CCSER1 knockout, researchers can investigate synthetic lethal interactions or vulnerability to therapies targeting mitotic machinery.
This product supports diverse research applications, including investigations into cytokinesis failure, cell cycle checkpoint aberrations, and microtubule dynamics in cancer. Representative assays include western blotting for CCSER1 and tubulin isoforms, immuno fluorescence staining of microtubule networks and midbody structures, flow cytometry for cell cycle distribution and polyploidy, and cytokinesis failure rate quantification. Further functional studies such as apoptosis assays and migration/invasion assays enable comprehensive profiling of tumor aggressiveness. The polyclonal CCSER1 knockout NCI-H1975 cells are suitable for drug response profiling with EGFR inhibitors, Aurora kinase inhibitors, or microtubule poisons. For detailed technical inquiries, please contact Ascent Research.
