The ADIPOR1 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the gene encoding adiponectin receptor 1 (ADIPOR1) has been targeted for disruption. This polyclonal format provides a mixed knockout pool derived from the HT29 human colorectal adenocarcinoma epithelial cell line, offering a versatile loss-of-function model for investigating ADIPOR1-dependent signaling without the selection of a single clonal isolate. The gene-edited population is designed for use in functional assays requiring abrogation of ADIPOR1-mediated responses, including metabolic studies, signal transduction analysis, and drug screening applications.
The HT29 parental cell line is an adherent epithelial model isolated from a 44-year-old female with colorectal adenocarcinoma. These cells retain the capacity to undergo enterocytic differentiation under appropriate culture conditions, making them a well-established system for studying intestinal epithelial biology, mucosal barrier function, and colorectal cancer pathology. The HT29 background thus provides a physiologically relevant context in which to assess the role of ADIPOR1 in intestinal epithelial homeostasis and malignant transformation.
ADIPOR1 encodes a high-affinity receptor for the adipokine adiponectin. Upon ligand binding, ADIPOR1 recruits the adaptor protein APPL1 and triggers downstream signaling cascades, most notably the AMP-activated protein kinase (AMPK) pathway. ADIPOR1-mediated AMPK activation promotes fatty acid oxidation, glucose uptake, and insulin sensitization via phosphorylation of key metabolic regulators such as acetyl-CoA carboxylase (ACC) and transcriptional modulation through PPAR?? and SIRT1. Additionally, ADIPOR1 signaling reduces intracellular ceramide levels, linking it to broader metabolic and anti-apoptotic effects. The receptor thus functions as a critical node connecting adiponectin to cellular energy homeostasis and metabolic control.
In HT29 colorectal cancer cells, ablation of ADIPOR1 disrupts the adiponectin?CAMPK axis, impairing metabolic regulation and potentially altering proliferative and survival pathways. This knockout model is particularly relevant for examining how adiponectin signaling influences colorectal cancer metabolism, given the emerging evidence of AMPK??s tumor-suppressive roles. The loss of ADIPOR1 may also affect the ability of HT29 cells to respond to metabolic stress, making this system valuable for dissecting the receptor??s contribution to energy sensing and mitochondrial function in a cancer context.
Typical applications include functional studies of ADIPOR1-dependent signaling using adiponectin stimulation followed by Western blot analysis of ADIPOR1 and phosphorylated AMPK, RT-qPCR for mRNA expression, and AMPK phosphorylation assays. The polyclonal knockout cells are also suitable for metabolic profiling via glucose uptake and fatty acid oxidation assays, as well as phenotypic analyses such as cell proliferation (MTT/colony formation), migration, and invasion assays. These cells can serve in drug screening for ADIPOR1 activators and in investigations of the AMPK pathway in colorectal cancer. For further technical information, please contact Ascent Research.
