The Ahr Knockout LLC Cell Line is a CRISPR/Cas9-edited knockout cell line derived from LLC (Lewis lung carcinoma) cells, featuring targeted disruption of the mouse Ahr gene. This product provides a stable loss-of-function model for investigating Ahr-mediated signaling pathways in a murine lung adenocarcinoma background. The knockout cell line offers a defined genetic background for mechanistic studies, without the need for transient silencing approaches. It is suitable for a wide range of assays examining Ahr-dependent cellular processes.
LLC cells, originally isolated from a C57BL/6 mouse lung epithelial carcinoma, represent a widely used syngeneic model of lung adenocarcinoma. These cells form aggressive tumors in immunocompetent mice and are extensively employed in cancer biology, metastasis research, and tumor immunology. Their responsiveness to xenobiotic compounds and their immunomodulatory properties make them particularly relevant for studying the intersection of environmental carcinogens and immune responses. The LLC background facilitates in vivo tumor studies in the C57BL/6 strain without immune rejection.
Ahr encodes a ligand-activated basic helix-loop-helix (bHLH)-PAS transcription factor. In the absence of ligand, Ahr resides in the cytoplasm complexed with HSP90, AIP, and p23. Upon binding ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), benzo[a]pyrene, or the endogenous tryptophan metabolite kynurenine, Ahr undergoes conformational change, translocates to the nucleus, and heterodimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT). This complex binds xenobiotic response elements (XREs) in target gene promoters, driving transcription of genes including CYP1A1, CYP1B1, IL-22, IL-17, and the Ahr repressor AHRR. Ahr thus regulates phase I xenobiotic metabolism, immune cell differentiation, and cell cycle control, integrating environmental and metabolic cues.
Disruption of Ahr in LLC cells abrogates ligand-induced transcriptional responses, enabling dissection of Ahr’s role in lung adenocarcinoma progression. Because Ahr influences both tumor cell-intrinsic properties and the surrounding microenvironment??including immune cell polarization and cytokine production??this knockout model facilitates examination of how loss of Ahr signaling affects tumor growth, metastasis, and immune evasion. It is particularly valuable for studying the link between aryl hydrocarbon receptor activity and the acquisition of malignant phenotypes in a lung cancer context.
Researchers can use the Ahr Knockout LLC Cell Line in diverse experimental settings. Xenobiotic metabolism studies can employ Western blotting for CYP1A1 induction or XRE-luciferase reporter assays. Immunological investigations may include flow cytometry for IL-22 or IL-17 expression, or co-culture models to assess effects on immune cell function. Tumor cell migration and drug sensitivity assays provide functional readouts of Ahr-dependent phenotypes. For further information, please contact Ascent Research.
