The ADAMTS14 Knockout Ca Ski Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population of the ADAMTS14 gene in the Ca Ski human cervical carcinoma cell line. This loss-of-function model enables researchers to investigate the functional consequences of ADAMTS14 deficiency in a well-characterized tumorigenic background. The product is supplied as a heterogeneous pool of gene-edited cells, providing a robust platform for studying ADAMTS14-dependent processes in extracellular matrix biology and cancer cell behavior.
The parental Ca Ski cell line originates from a metastatic lesion of a cervical epidermoid carcinoma to the small intestine and harbors an integrated human papillomavirus 16 (HPV16) genome. This cell line is a widely accepted model for HPV-driven cervical carcinogenesis and retains key oncogenic hallmarks, making it ideal for examining gene functions relevant to tumor progression and metastasis.
At the molecular level, ADAMTS14 encodes a procollagen N-proteinase that cleaves the N-propeptides of procollagens I, II, and III, a critical step in fibrillar collagen assembly. Its activity is regulated by upstream TGFB1, IL1B, and mechanical stress, while downstream targets include COL1A1, COL2A1, COL3A1, and mature collagen fibrils. ADAMTS14 interacts with collagen substrates, other ADAMTS family members, and matrix proteoglycans, and operates in the TGFB1?CSMAD2/3?CADAMTS14?Ccollagen fibril signaling axis. TGFB1-mediated SMAD2/3 signaling transcriptionally upregulates ADAMTS14, which in turn promotes procollagen processing, thereby modulating cell adhesion, migration, and ECM stiffness.
In the Ca Ski context, ADAMTS14 disruption impairs procollagen processing, leading to defective collagen fibril formation and altered ECM organization. This dysregulates focal adhesion dynamics, integrin signaling, and tumor microenvironment biomechanics. Consequently, knockout cells may exhibit altered invasive capacity, anoikis resistance, and paracrine interactions central to cervical cancer metastasis. The HPV16-positive background is particularly relevant as viral oncoproteins can intersect with ECM remodeling pathways, potentially revealing synergistic effects on malignant progression.
This polyclonal knockout product is suited for dissecting ECM remodeling in cervical cancer, evaluating collagen maturation defects, and screening therapeutic agents targeting ECM proteases. Common assays include Western blotting for procollagen processing, RT-qPCR for ADAMTS14 and COL1A1 expression, immunofluorescence for collagen fibril organization, Transwell invasion, collagen gel contraction, and zymography. This model enables mechanistic studies of tumor?Cstroma interactions and identification of novel vulnerabilities in metastatic cancer. For additional technical details and ordering, please contact Ascent Research.
