The BCL10 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of human colorectal adenocarcinoma cells with targeted disruption of the BCL10 gene. This loss-of-function model is supplied as a heterogeneous knockout pool, avoiding clonal selection to preserve the genetic diversity of the parental HT29 line. The cells provide a robust platform for investigating BCL10-dependent signaling in an epithelial context relevant to intestinal biology and colorectal cancer.
HT29 cells originate from a human colon carcinoma and display epithelial morphology, widely utilized to study intestinal epithelial barrier function, colorectal tumorigenesis, and mucosal immune responses. This cell line endogenously expresses components of the CBM signalosome and innate immune receptors, making it suitable for analyzing antigen receptor-like signaling pathways and NF-??B regulation in a carcinoma background.
As a core adaptor of the CARD11-BCL10-MALT1 (CBM) complex, BCL10 transduces signals from antigen receptors and immunoreceptors to the IKK complex. Upon CARD11-mediated activation and PKC?? phosphorylation, BCL10 oligomerizes with MALT1, engaging TRAF6 and NEMO (IKK??) to activate IKK. This triggers I??B?? phosphorylation and degradation, releasing NF-??B p65/p50 to induce transcription of IL-6, TNF??, and anti-apoptotic factors (Bcl-xL, c-FLIP). Disruption of BCL10 uncouples receptor stimulation from the IKK/NF-??B axis.
In colorectal adenocarcinoma, BCL10-driven NF-??B signaling promotes inflammation and apoptosis resistance, contributing to tumor progression. The HT29 background, with its characteristic APC and TP53 mutations, offers a disease-relevant context. BCL10 knockout impairs cytokine production and survival in response to IL-1 or Toll-like receptor stimulation. This model also explores how intestinal epithelial cells might adopt lymphoid-like CBM signaling, relevant to MALT lymphoma biology.
Applications include co-immunoprecipitation of CBM components (CARD11, MALT1, TRAF6), NF-??B luciferase reporter assays, Western blotting for phospho-I??B?? and p65, and RT-qPCR for IL-6 and TNF??. The pool supports drug screening for NF-??B pathway inhibitors, CRISPR editing validation, and apoptosis/proliferation studies using Annexin V and flow cytometry. For technical support, contact Ascent Research.
