The CCNYL1 Knockout NCI-H1975 Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the CCNYL1 gene in the human NCI-H1975 lung adenocarcinoma epithelial cell line. This loss-of-function model permits population-level analysis of cyclin Y-like 1 function, avoiding clonal biases and enabling robust functional studies. The cells are maintained under standard culture conditions and are compatible with a variety of downstream assays, providing a versatile platform for investigating CCNYL1-dependent mechanisms.
NCI-H1975 is a widely studied non-small cell lung cancer (NSCLC) line derived from the pleural effusion of a non-smoking female with metastatic adenocarcinoma. The line harbors activating EGFR mutations L858R and T790M, which are associated with EGFR tyrosine kinase inhibitor sensitivity and acquired resistance. It serves as a clinically relevant model for EGFR-mutant lung adenocarcinoma, recapitulating key features of advanced disease and oncogene addiction.
CCNYL1 encodes cyclin Y-like 1, a regulatory subunit that binds and activates CDK16. The CCNYL1?CCDK16 complex phosphorylates RB, releasing E2F transcription factors to drive expression of genes essential for G1/S transition. Transcription of CCNYL1 is itself regulated by E2F and MYC, establishing a feed-forward loop. Additionally, CCNYL1 interacts with CDK2, extending its potential influence on cell cycle progression. Thus, the CCNYL1?CCDK16?CRB?CE2F signaling axis is central to proliferative control, and its disruption is predicted to attenuate RB phosphorylation and E2F target gene induction.
Integrating CCNYL1 knockout into the NCI-H1975 background creates a powerful system to study cyclin-mediated regulation within an EGFR-driven context. Because EGFR signaling converges on MYC and E2F pathways, loss of CCNYL1 may uncover synthetic lethal vulnerabilities or compensatory mechanisms unique to EGFR-mutant tumors. This model enables precise interrogation of how oncogenic signaling co-opts cell cycle machinery, potentially revealing new intervention points for drug-resistant lung adenocarcinoma.
Typical research applications include cell cycle profiling by flow cytometry, proliferation and viability assays, immunoblotting, RT-qPCR, and co-immunoprecipitation to probe protein interactions. Genetic rescue experiments can confirm on-target effects, and the polyclonal population is well-suited for synthetic lethality screens and high-throughput studies. For further information, please contact Ascent Research.
