The ITGB6 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of A-549 human lung adenocarcinoma cells engineered to disrupt the ITGB6 gene, resulting in loss of integrin ??6 expression. This non-clonal, pooled format provides a genetically diverse loss-of-function model that minimizes clonal artifacts and is ideal for population-based functional studies.
A-549 is a non-small cell lung carcinoma line isolated from a 58-year-old male patient, exhibiting characteristics of alveolar Type II epithelial cells. Widely employed in cancer and fibrosis research, these adherent cells retain responsiveness to cytokines such as TGF-?? and TNF, enabling investigation of epithelial biology, integrin-mediated adhesion, and EMT in a relevant disease context.
ITGB6 encodes the ??6 integrin subunit that heterodimerizes with ??V to form ??v??6 integrin. This receptor binds fibronectin, vitronectin, and the LAP-TGF-??1 complex, mechanically activating latent TGF-??1. Activated TGF-??1 drives SMAD2 and SMAD3 phosphorylation and transcriptional programs. In parallel, ??v??6 ligation recruits FAK (PTK2) and SRC, stimulating downstream MAPK1/3 (ERK) and AKT signaling, and crosstalks with CTNNB1. ITGB6 expression is induced by TGFB1, TNF, EGF, via SMAD3, AP-1, and ETS1.
Knockout of ITGB6 in A-549 cells eliminates ??v??6 surface expression, impairing latent TGF-?? activation and attenuating SMAD-dependent transcription, FAK/SRC signaling, and ERK/AKT pathway activity. This model is especially powerful for discriminating integrin-dependent mechanisms in TGF-??-induced EMT and migration, and for studying the role of ??v??6 in lung cancer metastasis and fibrosis, including paracrine crosstalk with the tumor microenvironment.
Applications include investigation of integrin signaling, TGF-?? activation, focal adhesion biology, and screening of anti-??v??6 therapeutics. Representative assays are Western blot for phospho-SMAD2, total FAK, and AKT; RT-qPCR of EMT markers; flow cytometry for ??v??6; TGF-?? bioassay; scratch-wound and transwell migration; and adhesion to fibronectin. The polyclonal nature supports reproducible population-level data in drug screening. For additional information or customized products, contact Ascent Research.
