The HOMER1 Knockout A-549 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population derived from the human A-549 lung adenocarcinoma line, engineered for targeted disruption of the HOMER1 gene. As a polyclonal product, this population contains a heterogeneous mix of cells harboring various gene-disrupting edits, providing a genetically diverse loss-of-function model that avoids the selective pressures of clonal isolation. This format is ideal for robust, population-level studies of HOMER1 in a cancer cell context.
The A-549 cell line is a classic model of lung adenocarcinoma, originally derived from the tumor of a 58-year-old Caucasian male. These adherent epithelial cells retain key characteristics of cancerous lung epithelium, including dysregulated proliferation and migratory capacity, making them a standard tool for respiratory oncology and signal transduction research.
HOMER1 is a scaffold protein that directly links metabotropic glutamate receptor 5 (mGluR5) to inositol 1,4,5-trisphosphate receptors (IP3Rs) on the endoplasmic reticulum, mediating agonist-evoked calcium release. This calcium signal activates calcineurin-dependent NFAT and NF-??B transcription factors and intersects with the MAPK/ERK (ERK1/2) and PI3K/Akt pathways. HOMER1 forms complexes with Shank, Drebrin, PIKE, and TRPC1, and participates in actin cytoskeleton remodeling via Rho GTPases. Its expression is regulated by BDNF, Wnt signaling, and glutamate, situating it at the convergence of synaptic-like and oncogenic signaling cascades.
In A-549 cells, HOMER1-mediated calcium oscillations influence tumor cell behavior. Knockout of HOMER1 is predicted to disrupt IP3R-dependent calcium flux, attenuate NF-??B and ERK1/2 activation, and impair cytoskeletal organization. These changes may reduce proliferation and migration, underscoring the model’s relevance for dissecting HOMER1’s role in lung adenocarcinoma progression and metastasis.
This polyclonal knockout population is well-suited for a variety of experimental approaches, including Boyden chamber migration assays, MTT/CCK-8 proliferation analysis, and calcium imaging. Additional techniques such as western blotting, RT-qPCR, co-immunoprecipitation, and RNA-seq enable comprehensive characterization of HOMER1 disruption and its downstream effects. The model supports drug target validation and screening of inhibitors targeting HOMER1-mediated interactions. For further information, please contact Ascent Research.
