The KMT2C knockout A-549 polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human A-549 lung adenocarcinoma line. This pool enables loss-of-function studies of KMT2C, a histone methyltransferase involved in chromatin remodeling and transcription. The polyclonal format provides a heterogeneous population, minimizing clonal artifacts while ensuring functional gene disruption. This model is ideal for investigating KMT2C tumor suppressor roles.
The A-549 cell line is derived from a lung adenocarcinoma of an adult male and is a widely used model for alveolar type II epithelium. These cells exhibit constitutive activation of Wnt signaling and express wild-type p53, making them particularly relevant for studying tumor suppressor pathways. The polyclonal knockout population preserves these features while eliminating KMT2C, enabling direct assessment of its role in lung cancer biology.
KMT2C (MLL3) is a histone methyltransferase that catalyzes mono-, di-, and trimethylation of histone H3 at lysine 4, serving as a transcriptional coactivator. It functions within the COMPASS-like complex, interacting with ASH2L, RBBP5, WDR5, and DPY30. Recruitment by p53 and ??-catenin enables KMT2C to activate key tumor suppressor genes such as CDKN1A (p21) and BAX, along with HOX genes and Wnt target genes. Disruption of KMT2C impairs p53-dependent cell cycle arrest and apoptosis, while altering Wnt/??-catenin-driven transcription through TCF/LEF factors.
In the A-549 context, loss of KMT2C disrupts p53-mediated tumor suppression by reducing expression of CDKN1A and BAX, leading to diminished apoptosis and unchecked proliferation under genotoxic stress. Additionally, KMT2C deficiency may potentiate Wnt/??-catenin target gene expression through TCF/LEF, promoting oncogenic transcriptional programs. This polyclonal knockout model thus provides a powerful system to study epigenetic vulnerabilities and tumor suppressor mechanisms in lung adenocarcinoma.
Researchers can employ this polyclonal pool in Western blotting and ChIP-qPCR to assess KMT2C loss and H3K4 methylation changes, RT-qPCR and RNA-seq for transcriptomic profiling, flow cytometry for apoptosis and cell cycle analysis, and migration/invasion assays. Drug sensitivity screening can identify compounds targeting KMT2C-deficient cells. This product supports cancer epigenetics research, target validation, and drug discovery. For further information, please contact Ascent Research.
