The ADAMTS14 Knockout NCI-H1299 Polyclonal Cells represent a CRISPR/Cas9-edited human polyclonal knockout cell population, featuring targeted disruption of the ADAMTS14 gene in the NCI-H1299 non-small cell lung carcinoma cell line. This loss-of-function model enables systematic investigation of ADAMTS14-mediated procollagen processing and its contribution to extracellular matrix (ECM) dynamics in a metastatic lung cancer background. The polyclonal format preserves population-level heterogeneity, allowing researchers to assess gene function in a context that reflects the complexity of tumor cell populations.
The NCI-H1299 cell line was established from a lymph node metastasis of a human non-small cell lung carcinoma, representing a widely used model of aggressive, p53-deficient lung cancer. These cells exhibit metastatic potential and are extensively employed to study tumor progression, invasion, and microenvironmental interactions. The p53-null status of NCI-H1299 cells further accentuates genomic instability and alters cellular responses to stress, providing a clinically relevant substrate for probing the role of ADAMTS14 in cancer pathogenesis.
ADAMTS14 encodes a secreted procollagen N-proteinase that specifically cleaves the N-propeptides of procollagens I and II, thereby regulating the assembly and maturation of collagen fibrils. Its activity is tightly controlled by upstream regulators including TGF-?? signaling, inflammatory stimuli, and mechanical stress. Downstream, ADAMTS14 processes collagen type I and type II, influencing ECM composition and structural integrity. The enzyme interacts directly with collagen types I, II, and III, thrombospondin-1, and matrix metalloproteinases, and its function is integrated into pathways involving TGF-?? and integrin-mediated cell surface interactions. Disruption of ADAMTS14 therefore decouples procollagen processing from fibrillogenesis, leading to defective collagen scaffold formation.
In the NCI-H1299 metastatic lung cancer model, knockout of ADAMTS14 is predicted to perturb the tumor stroma by impairing collagen maturation and organization, thereby altering cell adhesion, migration, and invasion. Given that NCI-H1299 cells lack functional p53, this knockout model permits dissection of how ECM remodeling intersects with genomic instability to drive metastatic dissemination. The aberrant collagen network may compromise integrin-mediated mechanotransduction and stromal crosstalk, potentially attenuating tumor-stroma interactions critical for metastatic niche formation.
Researchers can employ the ADAMTS14 Knockout NCI-H1299 Polyclonal Cells to investigate ECM remodeling mechanisms underlying lung cancer metastasis, assess the contribution of ADAMTS14 to tumor cell invasion and migration, and screen anti-fibrotic or anti-metastatic compounds. Suitable assays include western blotting to monitor collagen I and II processing, immunofluorescence to visualize collagen fiber architecture, RT-qPCR to quantify matrix-associated gene expression, and transcriptomic profiling via RNA-seq to map global ECM changes. These cells also support functional studies examining how ADAMTS14-dependent collagen modifications modulate integrin signaling and cell motility. For further information, please contact Ascent Research.
