The ADAMTS14 Knockout T-47D Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout population of the T-47D human breast ductal carcinoma cell line, engineered to disrupt the ADAMTS14 gene. This polyclonal format avoids clonal artifacts and captures a broad spectrum of editing events, ensuring a robust loss-of-function model. By abolishing ADAMTS14 expression, these cells allow precise investigation of its role in procollagen processing and extracellular matrix (ECM) dynamics.
T-47D cells were originally isolated from a pleural effusion of a human breast ductal carcinoma and display adherent epithelial morphology with hormone-responsive signaling. As a well-characterized breast cancer model, they retain estrogen and progesterone receptor pathways, making them especially relevant for studying hormone-driven ECM alterations. Their metastatic origin further enhances their utility in tumor invasion and dissemination research.
ADAMTS14 encodes a secreted metalloprotease that cleaves aminopropeptides from fibrillar procollagens, including COL1A1, COL2A1, and COL3A1, a critical step for mature collagen fibril formation. Its expression is activated by TGFB1 and IL1B and is integrated into the TGF-beta signaling cascade through interactions with SMAD2/3. ADAMTS14 associates with matrix molecules such as fibronectin (FN1) and perlecan (HSPG2) and is inhibited by TIMP3, positioning it at the nexus of growth factor signaling and ECM structural integrity.
In the T-47D context, knockout of ADAMTS14 is predicted to impair procollagen aminopropeptide cleavage, leading to defective collagen assembly and compromised ECM architecture. This disruption likely alters cell adhesion, migration, and invasion??processes central to breast cancer progression. Given the hormone-responsive nature of T-47D, this model enables dissection of the interplay between hormonal signals and matrix remodeling, and how ECM changes influence tumor microenvironment properties such as stiffness and cytokine presentation.
This knockout tool is suited for a diverse array of research applications, including western blotting and mass spectrometry for collagen processing, collagen gel contraction and immunofluorescence for ECM organization, Transwell assays for migration and invasion, and in vivo tumor xenograft models for metastasis studies. It serves as a valuable platform for validating matrix-targeted therapeutics and exploring ADAMTS14 function in breast cancer metastasis. For further technical inquiries, please contact Ascent Research.
