The CAV2 Knockout NCI-H1299 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of NCI-H1299 non-small cell lung cancer (NSCLC) cells carrying disruptive mutations in the CAV2 gene. This heterogeneous knockout model eliminates the need for single-cell cloning and enables population-level analyses of caveolin-2 loss-of-function phenotypes in a human lung adenocarcinoma context.
The NCI-H1299 cell line is derived from a lymph node metastasis of a male patient with lung adenocarcinoma. It features a p53-null and p16-deficient genotype, lacking functional TP53 and CDKN2A tumor suppressors. This genetic background facilitates the study of aggressive oncogenic signaling and metastatic processes.
Caveolin-2 (CAV2) forms hetero-oligomers with CAV1 essential for caveolae biogenesis and scaffolds signaling molecules such as SRC, EGFR, and eNOS. CAV2 modulates the MAPK/ERK and PI3K/AKT pathways by inhibiting SRC-dependent EGFR phosphorylation and eNOS activity. Expression is regulated by TGF-??, PDGF, oxidative stress, and HIF-1??, while interacting partners include integrin ??1 and PTRF/cavin-1.
CAV2 knockout in NCI-H1299 cells is particularly relevant for studying caveolin-dependent regulation of lung adenocarcinoma progression. The p53-null/p16-deficient background, combined with CAV2 ablation, allows dissection of EGFR and SRC pathway contributions to proliferation, survival, and migration. This model also supports investigation of caveolae-mediated endocytosis and its impact on drug delivery and metastasis.
Applications include Western blotting, RT-qPCR, immunofluorescence, wound healing, transwell invasion, and MTT assays to assess CAV2 expression and cellular functions. Phospho-ERK/AKT analysis and co-immunoprecipitation with SRC or EGFR can delineate signaling changes. The polyclonal pool is suitable for xenograft tumor growth studies to evaluate metastasis. For further technical inquiries, please contact Ascent Research.
