The IL17RB Knockout HT29 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout population of the HT29 human colorectal adenocarcinoma cell line, carrying targeted disruption of the IL17RB gene. IL17RB encodes interleukin-17 receptor B, a receptor for the cytokines IL17B and IL25 (IL-17E) that mediates pro-inflammatory and allergic signaling cascades. This polyclonal knockout model provides a powerful loss-of-function tool for dissecting IL17B/IL25-driven signaling networks in a physiologically relevant epithelial cancer background without the need for single-cell cloning.
The HT29 cell line is a well-characterized human colorectal adenocarcinoma model originally derived from a primary colon adenocarcinoma of a 44-year-old female. These cells exhibit epithelial morphology and have been extensively employed in basic and translational research to study colorectal cancer biology, intestinal epithelial barrier function, drug absorption, and therapeutic response. HT29 cells retain intact inflammatory signaling circuitry, including components of the NF-??B and JAK-STAT pathways, making them an appropriate host for investigating IL17RB-mediated cytokine responses in the context of colorectal malignancy.
At the molecular level, IL17RB functions as a transmembrane receptor that heterodimerizes with IL17RA upon binding its ligands IL17B or IL25. The activated receptor complex recruits the adaptor protein ACT1 (TRAF3IP2/CIKS), which engages TRAF6 and TAK1, leading to activation of the IKK complex and phosphorylation of NF-??B p65, as well as JNK-mediated AP-1 signaling. Additionally, IL17RB stimulation can trigger JAK1/2-dependent phosphorylation of STAT3. These convergent signals drive transcriptional upregulation of pro-inflammatory cytokines such as IL-6, IL-8, and TNF-??, and chemokines including CXCL1 and CXCL2. Expression of IL17RB itself is modulated by TNF-?? and IL-1??, integrating with NF-??B and JAK-STAT networks.
In the HT29 colorectal adenocarcinoma background, IL17RB-mediated signaling is implicated in shaping the inflammatory tumor microenvironment. Knockout of IL17RB in these cells is expected to disrupt the autocrine and paracrine cytokine loops that depend on IL17B/IL25, thereby altering the secretion of key inflammatory mediators and potentially affecting tumor cell behaviors such as proliferation, survival, and migration. This model is therefore highly relevant for studies linking chronic inflammation to colorectal cancer progression and for evaluating the contribution of IL17RB to immune evasion and stromal crosstalk within the intestinal epithelium.
Researchers can employ this polyclonal knockout model to interrogate IL17RB-dependent signaling pathways in colorectal cancer, assess the impact on pro-inflammatory cytokine production via ELISA or multiplex assays, and perform phospho-signaling analyses (e.g., phospho-STAT3, phospho-p65) to map downstream effector activation. It is also suited for drug sensitivity screens against anti-inflammatory or targeted agents, evaluation of tumor cell migration and invasion in Transwell assays, and mechanistic studies of allergic inflammation using asthma-relevant stimuli. This CRISPR/Cas9-edited polyclonal knockout population serves as a versatile platform for both mechanistic dissection and therapeutic discovery. For further information, please contact Ascent Research.
