The ELANE Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the human ELANE gene. CRISPR/Cas9 technology was used to introduce targeted disruptions in the ELANE locus, resulting in a heterogeneous pool of LoVo colorectal adenocarcinoma cells lacking neutrophil elastase expression. This polyclonal format ensures representation of diverse editing outcomes, reflecting genetic heterogeneity relevant to tumor biology and enabling functional studies without clonal selection bias.
LoVo cells were derived from a lymph node metastasis of a colon adenocarcinoma patient and serve as a classical in vitro model for colorectal cancer. They retain invasive characteristics and responsiveness to inflammatory mediators, making them well-suited for investigating extracellular matrix interactions and metastatic mechanisms central to ELANE function. These cells are extensively characterized and widely used for cancer drug screening and metastasis research, expressing relevant adhesion molecules and producing matrix metalloproteinases that complement the study of ELANE-mediated matrix degradation.
ELANE encodes neutrophil elastase, a serine protease that degrades elastin, collagen, and fibronectin within the extracellular matrix. Its transcription is regulated by transcription factors CEBPE and PU.1, and expression is inducible by cytokines IL-8 and TNF-??. Active elastase promotes cytokine activation and interacts with CD11b/CD18 integrin, while its activity is inhibited by SERPINA1. In signaling networks, ELANE operates downstream of TLR4 and participates in IL-8-driven neutrophil extracellular trap formation and inflammatory amplification. Additionally, ELANE-mediated cleavage of ECM components releases bioactive fragments that modulate TLR4 signaling, amplifying inflammatory responses, and the enzyme processes pro-inflammatory cytokines, further linking innate immunity to cancer progression.
In the LoVo colon adenocarcinoma context, ELANE knockout abolishes matrix-degrading activity, potentially suppressing tumor cell invasion and disrupting pro-inflammatory feedback loops in the tumor microenvironment. This model allows dissection of elastase-dependent pathways without confounding effects from immune cell-derived enzyme, distinguishing its specific contributions from those of other proteases like matrix metalloproteinases. The polyclonal nature minimizes clonal artifacts and supports the study of invasion mechanisms under more physiologically relevant, heterogeneous conditions, which is critical when evaluating therapeutic strategies.
This product supports applications such as studying neutrophil elastase in colorectal cancer invasion, screening ELANE inhibitors, and analyzing inflammation-mediated tumor progression. Compatible assays include Western blotting, elastase activity measurements, migration/invasion assays, cytokine ELISA, immunofluorescence for ECM components, and xenograft tumor studies. These cells are supplied as a growing polyclonal population and can be used directly in functional assays, with routine validation by sequencing or Western blot to confirm loss of ELANE protein expression. For detailed protocols and batch-specific data, please contact Ascent Research.
