The EFEMP2 Knockout HCT 116 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the EFEMP2 gene has been disrupted. This polyclonal knockout cell model is generated from the HCT 116 host cell line and serves as a loss-of-function tool for investigating EFEMP2-dependent biological processes without the limitations of single-cell clonal selection.
The host cell line, HCT 116, is a well-characterized human colorectal carcinoma epithelial cell line harboring a KRAS G13D mutation and exhibiting microsatellite instability-high (MSI-H) status. This cell line retains key features of intestinal epithelial cells and is widely employed as a model for colorectal cancer biology, including studies of intestinal barrier function, oncogenic signaling, and tumor microenvironment interactions. The HCT 116 background provides a clinically relevant context for examining the functions of extracellular matrix (ECM)-associated genes in cancer progression.
EFEMP2 encodes fibulin-4, an extracellular matrix glycoprotein indispensable for elastic fiber assembly. Fibulin-4 interacts with tropoelastin, fibrillin-1, and LTBP-2, and facilitates crosslinking of tropoelastin by lysyl oxidase (LOX), a process essential for elastogenesis and tissue elasticity. Moreover, fibulin-4 modulates TGF-beta signaling by regulating the bioavailability of latent TGF-beta complexes through its binding to LTBP-2 and fibrillin-1, placing it upstream of TGFBR2 and SMAD2/3 activation. This protein is transcriptionally upregulated by TGFB1 and mechanical stretch, and in turn influences the expression of downstream targets such as ELN, FBN1, CTGF, and COL1A1. Through these interactions, EFEMP2 orchestrates a signaling network that balances ECM deposition and growth factor responses.
In the HCT 116 colorectal carcinoma background, disruption of EFEMP2 is particularly relevant for studying TGF-beta-driven EMT, ECM remodeling, and tumor cell invasion. Aberrant TGF-beta signaling is a hallmark of colorectal cancer progression, and fibulin-4??s role in sequestering cytokines and organizing elastic fiber components suggests that its loss may alter integrin-mediated adhesion, matrix stiffness, and cell migration. Thus, this polyclonal knockout population offers a valuable model for dissecting how fibulin-4 deficiency perturbs the tumor microenvironment and influences cancer cell behavior.
Typical research applications include quantitative analysis of TGF-beta pathway activation via phospho-SMAD2/3 assays, evaluation of ECM protein expression by western blotting and immunofluorescence, and functional assessment of migratory and invasive capacity using transwell migration/invasion assays. The cells are also suitable for cell proliferation studies and for screening compounds that may correct elastic fiber dysfunction associated with cutis laxa type IB. Additional uses encompass exploring the crosstalk between ECM integrity and KRAS-driven oncogenic signaling in MSI-H tumors. For further details on the EFEMP2 Knockout HCT 116 Polyclonal Cells, please contact Ascent Research.
