The MALT1 Knockout PC-9(Luciferase) Cell Line is a CRISPR/Cas9-edited knockout model derived from the human lung adenocarcinoma PC-9(Luciferase) line, featuring targeted disruption of the MALT1 gene. MALT1 encodes a paracaspase that functions as an adaptor and protease in the CARD11-BCL10-MALT1 (CBM) signaling complex. This knockout cell line provides a stable, loss-of-function system for investigating MALT1-dependent pathways.
The host PC-9(Luciferase) line is a human lung adenocarcinoma epithelial cell line harboring an in-frame EGFR exon 19 deletion, a common oncogenic driver in NSCLC, and stably expresses luciferase enabling non-invasive bioluminescence imaging in animal models. This well-characterized line is extensively used for investigating EGFR-targeted therapy sensitivity and resistance, as well as ancillary pathway contributions to tumor biology.
MALT1 acts as a paracaspase within the CBM signalosome, linking antigen receptor and innate immune activation to NF-??B-driven inflammatory gene expression. Upstream signals from TCR, BCR, or PKC engage CARD11, which nucleates a complex with BCL10 and MALT1. MALT1 interacts with BCL10, TRAF6, and NEMO, and its proteolytic activity cleaves A20, CYLD, and other substrates, while modulating IKK??/IKK??/IKK?? kinase activity. This culminates in phosphorylation and degradation of I??B, releasing NF-??B p65/p50 dimers to induce target genes such as A20, Regnase-1, and inflammatory mediators. In this manner, MALT1 integrates upstream immune stimuli into transcriptional programs regulating survival, proliferation, and inflammation.
In the PC-9 EGFR-mutant context, MALT1 knockout likely disrupts CBM-dependent NF-??B activation, potentially impairing pro-survival signaling and inflammatory responses that support tumor maintenance. Crosstalk between EGFR and NF-??B pathways is implicated in acquired resistance and tumor aggressiveness; thus, MALT1 loss may alter cell viability, apoptosis sensitivity, and migratory capacity. This model enables dissection of MALT1-mediated signaling in lung adenocarcinoma, clarifying its contributions to inflammation-driven tumor progression.
Key applications include Western blotting for MALT1 and downstream targets, NF-??B luciferase reporter assays, cell viability (MTT) and apoptosis (Annexin V) analyses, and Transwell migration assays. In vivo, bioluminescence imaging allows longitudinal monitoring of tumor xenografts. This knockout line supports studies on MALT1-dependent drug sensitivities, the role of chronic inflammation in EGFR-mutant lung cancer, and CBM complex contributions to tumor microenvironment signaling. For technical support or product inquiries, contact Ascent Research.
