IL17RB Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma cell line LoVo, in which the gene encoding the interleukin-17 receptor B (IL17RB) has been disrupted via non-homologous end joining-mediated gene editing. This polyclonal pool contains a heterogeneous mix of edited alleles, providing a loss-of-function model for investigating IL17RB-dependent signaling pathways. The product serves as a ready-to-use reagent for functional genomics studies without the need for single-cell cloning, ensuring a representative, polyclonal gene disruption suitable for population-based assays.
The LoVo host cell line was established from a metastatic lymph node of a 56-year-old male patient with colon adenocarcinoma and is widely employed as a model for colorectal cancer metastasis, invasion, and epithelial biology. LoVo cells retain key characteristics of aggressive colorectal cancer, including deregulated adhesion, enhanced motility, and intrinsic resistance to certain chemotherapeutic agents. Their well-characterized genetic background and robust growth in vitro make them an optimal choice for studying tumor cell behavior and for evaluating the contribution of specific genes to metastatic progression.
IL17RB encodes a transmembrane receptor that binds the pro-inflammatory cytokines IL-17B and IL-25 (IL-17E), forming heterodimers with the co-receptor IL17RA and initiating intracellular cascades. Upon ligand engagement, the adaptor protein TRAF3IP2 (Act1) is recruited, facilitating ubiquitination of TRAF6 and subsequent activation of the kinase TAK1. This leads to downstream activation of the NF-??B and MAPK/ERK pathways, which transcriptionally regulate a panel of pro-inflammatory and pro-survival targets, including CXCL8 (IL-8), CCL20, MMP9, and BCL2L1. Additional upstream regulators such as TNF-alpha can modulate IL17RB expression or synergize with its signals. The receptor also interfaces with the JAK/STAT axis, particularly STAT3, contributing to Th2-type immune responses and chronic inflammatory conditions.
Disruption of IL17RB in LoVo cells abrogates IL-17B- and IL-25-triggered signaling, resulting in diminished NF-??B and MAPK pathway activity. This attenuation correlates with reduced transcription of CXCL8 and CCL20, weakened matrix metalloproteinase (MMP9) production, and impaired cell migration and invasion. Consistent with the gene??s mechanistic role, the knockout model exhibits decreased proliferation and enhanced susceptibility to apoptosis, highlighting the reliance of colorectal cancer cells on IL17RB for maintenance of aggressive phenotypes. These features render the polyclonal knockout cells a physiologically relevant system for dissecting cytokine-driven tumor microenvironment interactions and for identifying IL17RB-dependent vulnerabilities in colorectal cancer.
Researchers can employ IL17RB Knockout LoVo Polyclonal Cells for a wide array of applications, including functional dissection of IL-17 receptor biology in colon cancer, systematic screening of pharmacological inhibitors targeting IL17RB, and investigation of inflammatory signaling contributions to drug resistance. Western blotting of phospho-p65 and phospho-ERK, coupled with RT-qPCR analysis of IL17RB, CXCL8, and CCL20, allows quantitative assessment of pathway inhibition. Functional assays such as transwell migration/invasion, MTT proliferation, and Annexin V apoptosis assays further validate the role of IL17RB in tumor cell behavior. Additionally, the cells are compatible with NF-??B luciferase reporter and cytokine bead array platforms, facilitating high-throughput mechanistic and compound profiling studies. For further details or technical support, please contact Ascent Research.
