The INHBE Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population carrying targeted disruption of the INHBE gene in the LoVo human colorectal adenocarcinoma cell line. This polyclonal knockout cell pool is generated by CRISPR/Cas9-mediated gene disruption, resulting in a loss-of-function model that avoids clonal selection bias. It is ideally suited for population-level functional assays that require biological replicates and robust statistical power.
The LoVo cell line was established from a metastatic lymph node of a colon adenocarcinoma and is a widely characterized model for colorectal cancer progression. LoVo cells exhibit prominent invasive and migratory capabilities and are routinely used to investigate chemosensitivity, metastatic dissemination, and tumor biology. As a host for gene knockout, LoVo provides a clinically relevant platform to study INHBE in a colorectal adenocarcinoma context, linking intrinsic malignancy traits with perturbations in metabolic and signaling pathways.
INHBE encodes the inhibin beta E subunit, which dimerizes with the inhibin alpha subunit (INHA) to form inhibin E, a member of the TGF-?? superfamily. This heterodimer signals through type I and II TGF-?? receptors (ACVR1, ACVR2B) to activate SMAD2/3 phosphorylation. As a hepatokine, inhibin E regulates insulin sensitivity and glucose metabolism, intersecting with the insulin receptor substrate IRS1?CAKT pathway and modulating FOXO1-dependent transcription of gluconeogenic enzymes such as G6PC and PCK1. INHBE expression is responsive to insulin, glucagon, high-fat diet, PPARalpha, and TGF-??, placing it at a nexus of metabolic and growth factor signaling.
In the tumor microenvironment, INHBE may influence cancer cell proliferation, migration, and metabolic reprogramming. Disruption of INHBE in LoVo cells allows dissection of its role in modulating insulin sensitivity and TGF-?? family signaling within a colorectal cancer framework. The polyclonal nature of the knockout pool ensures that the cellular heterogeneity inherent in tumor cell populations is retained, enabling more physiologically relevant studies of drug responses and invasive behavior compared to single-cell clones. This model is particularly valuable for examining how INHBE loss impacts the crosstalk between metabolism and oncogenic signaling.
Typical applications include western blotting for INHBE and phospho-SMAD2/3, RT-qPCR analysis of downstream targets like G6PC and PCK1, MTT and Transwell assays for proliferation and migration, apoptosis detection, and glucose uptake measurements. Insulin signaling phospho-analysis and transcriptome-wide RNA-seq further delineate the network linking INHBE to metabolic enzymes and transcription factors such as FOXO1. For technical details or to discuss custom gene-editing projects, please contact Ascent Research.
