The EFEMP1 Knockout A-549 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma epithelial cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption of EFEMP1, resulting in a heterogeneous cell population with targeted gene ablation. The polyclonal nature offers a biologically relevant representation of gene knockout effects across a diverse cellular background, avoiding clonal artifacts. This product is suited for functional genomics studies examining EFEMP1-dependent signaling, extracellular matrix (ECM) interactions, and tumor-suppressive mechanisms in non-small cell lung cancer (NSCLC) research.
A-549 cells were originally isolated from the lung adenocarcinoma of a 58-year-old male and serve as a widely used model for NSCLC and alveolar epithelial biology. These adherent epithelial cells retain key features of type II pulmonary epithelium, including the ability to process surfactant and form polarized monolayers. Their robust growth characteristics and genetic tractability make them ideal for CRISPR/Cas9 editing and subsequent phenotypic analyses. The EFEMP1 knockout background in this context enables direct investigation of fibulin-3 function within an established lung cancer cell environment, contributing to our understanding of adenocarcinoma progression and ECM remodeling.
EFEMP1 encodes fibulin-3, a secreted glycoprotein that integrates into the ECM and modulates cell adhesion, migration, and tissue homeostasis. Fibulin-3 interacts with laminin, fibronectin, tropoelastin, and integrins, and it is regulated by upstream factors such as TGF-beta, HIF-1alpha, EGF, SP1, and AP-1. Downstream, EFEMP1 influences FAK, Akt, and ERK phosphorylation cascades, which converge on transcription factors that control VEGF expression. The protein also forms complexes with TIMP3 and MMPs, connecting ECM integrity with proteolytic remodeling and angiogenesis. In signaling terms, EFEMP1 acts as a negative regulator of PI3K-Akt, MAPK, and TGF-beta pathways, and its loss disrupts integrin-mediated adhesion signaling, often via ITGA/ITGB heterodimers, Src, and mTOR.
In the A-549 cellular context, EFEMP1 is proposed to function as a tumor suppressor whose expression normally restricts malignant behaviors. Knocking out EFEMP1 in these lung adenocarcinoma cells is expected to relieve suppression of cell migration, invasion, and survival signaling, making this model highly relevant for dissecting mechanisms of NSCLC progression. The polyclonal knockout population facilitates studies on ECM-mediated tumor suppression, epithelial?Cmesenchymal transition, and angiogenic switch, all of which are critical in lung cancer pathology. Researchers can use this system to explore how fibulin-3 loss alters cellular responses to pro-inflammatory cytokines or hypoxic stress, providing a platform for identifying therapeutic vulnerabilities.
This knockout product supports a wide range of experimental applications, including functional rescue assays, transcriptomic profiling by RNA-seq, and phospho-kinase array analysis to map altered signaling networks. Typical downstream assays include western blotting, RT-qPCR, migration and invasion assays, cell adhesion and proliferation measurements, immunofluorescence for ECM organization, and flow cytometry to quantify integrin surface expression. It is also well-suited for drug sensitivity screens and co-culture experiments that probe tumor?Cstroma interactions. For further information or inquiries about custom utilization, please contact Ascent Research.
