The CASZ1 Knockout NCI-H1299 Polyclonal Cells constitute a polyclonal cell population derived from the NCI-H1299 human lung carcinoma line, engineered using CRISPR/Cas9-mediated gene disruption to ablate CASZ1 function. This product provides a mixed pool of edited cells, avoiding the clonal biases associated with single-cell-derived lines, and is suitable for studying the collective loss-of-function effects of this zinc finger transcription factor in a relevant carcinoma background.
NCI-H1299 is a well-established cell model originating from a lymph node metastasis of a non-small cell lung carcinoma (NSCLC). Its epithelial origin and metastatic derivation make it particularly suited for examining molecular mechanisms of lung cancer progression, invasion, and therapeutic resistance. The cell line retains features of lung epithelial cells and is frequently employed to investigate signaling pathways dysregulated in lung carcinogenesis.
CASZ1 encodes a zinc finger transcription factor that directly binds DNA to regulate genes controlling cell fate determination and cytoskeletal dynamics. It is transcriptionally regulated by TGF-?? superfamily ligands, including BMPs, and cooperates with factors such as GATA4, BRG1 (SMARCA4), and SMAD2/3. CASZ1 functions as a repressor of MYCN and REST, while promoting expression of RhoB, E-cadherin, and BMP4. Through these interactions, CASZ1 integrates signals from the BMP and Wnt pathways, where Wnt3a acts upstream, to maintain epithelial integrity and restrict invasive behavior.
Disruption of CASZ1 in the NCI-H1299 background creates a relevant loss-of-function model to dissect its tumor suppressor role in lung carcinoma. Given the aggressive, metastatic nature of the parental line, abrogation of CASZ1-mediated repression of MYCN and REST, combined with attenuated RhoB signaling, is expected to promote epithelial-mesenchymal transition and enhance migratory capacity. This polyclonal population thus enables investigation of how CASZ1 deficiency re-wires transcriptional programs and signaling networks to drive NSCLC progression.
Researchers can utilize these cells for a wide range of functional assays, including transcriptomic profiling by RT-qPCR to validate CASZ1 target genes such as MYCN and RhoB, western blotting to monitor protein-level changes in downstream effectors, and transwell migration assays to quantify metastatic potential. Immunofluorescence staining for focal adhesions and ChIP-qPCR for CASZ1 binding sites further enable mechanistic dissection. These applications make the product a powerful tool for studying transcriptional regulation in lung cancer and for screening chemical or genetic modifiers that restore tumor suppressive pathways. For additional technical details or to request a quotation, please contact Ascent Research.
