HOXC11 Knockout A-549 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population derived from the A-549 lung adenocarcinoma cell line. This product introduces targeted disruption of the HOXC11 gene, generating a loss-of-function model for studying this homeobox transcription factor in a human epithelial cancer context. The polyclonal pool comprises a heterogeneous array of edits, avoiding single-cell cloning and providing a robust population-level readout ideal for signaling studies and phenotypic screens.
The parental A-549 cell line originates from a 58-year-old male with lung adenocarcinoma and displays adherent epithelial morphology. As a widely used model for non-small cell lung cancer (NSCLC), A-549 cells retain alveolar type II characteristics and express wild-type KRAS, making them a relevant system for dissecting oncogenic pathways and tumor progression.
HOXC11 encodes a homeodomain transcription factor that regulates development, differentiation, proliferation, and apoptosis. In cancer, it is frequently overexpressed and acts downstream of Wnt/??-catenin signaling: Wnt ligands (e.g., Wnt3a) engage Frizzled receptors, leading to ??-catenin stabilization and TCF/LEF-dependent transcription of HOXC11. HOXC11 subsequently activates target genes that drive invasion, EMT, and growth, including MMP2, MMP9, CCND1, MYC, and CDH2. Its transcriptional specificity is enhanced by interactions with PBX1, MEIS1, and PREP1 cofactors. Additional regulatory inputs from TGF-??, PI3K/AKT, and MAPK/ERK pathways converge on HOXC11, further fine-tuning its expression.
Disruption of HOXC11 in A-549 cells abrogates its transcriptional activity, resulting in downregulation of pro-proliferative and pro-invasive targets. This knockout model is expected to dampen Wnt/??-catenin-driven oncogenic signaling, reduce EMT marker expression, and impair invasive capacity. Given HOXC11??s role in lung adenocarcinoma metastasis, these cells are a powerful tool for investigating HOXC11-dependent tumor aggression and testing the reliance of A-549 cells on this factor for anchorage-independent growth, migration, and apoptosis resistance.
HOXC11 Knockout A-549 Polyclonal Cells are applicable to a broad range of assays. Proliferation can be measured by MTT, migration and invasion by Transwell, and apoptosis by Annexin V/PI staining. Transcriptional changes are quantifiable by RT-qPCR or RNA-seq, while downstream target occupancy can be assessed via ChIP-qPCR. Protein-level validation is achievable through Western blotting and immunofluorescence. These cells are suited for functional genomics, drug target validation, and HOX network analysis in lung cancer. For further information, please contact Ascent Research.
