The B4GALT1 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the LoVo human colorectal adenocarcinoma cell line, engineered for loss-of-function studies of B4GALT1. This polyclonal knockout pool, generated via CRISPR-mediated gene disruption, provides a heterogeneous model for investigating glycosylation-dependent processes without clonal selection artifacts.
The parental LoVo cell line was established from a metastatic lymph node of a colorectal adenocarcinoma patient, displaying an epithelial phenotype and widely used in colorectal cancer invasion, metastasis, and drug resistance research. These cells are well-characterized for adhesion properties and growth factor responsiveness, making them an ideal platform to assess the impact of glycosyltransferase ablation in a metastatic background.
B4GALT1 encodes a Golgi-resident beta-1,4-galactosyltransferase that transfers galactose from UDP-galactose to terminal N-acetylglucosamine on N- and O-glycans and glycolipids. With alpha-lactalbumin (LALBA), it forms lactose synthase for lactose production. B4GALT1 expression is regulated by transcription factor Sp1 and modulated by EGF and TGF-beta. Its galactosylation activity modifies downstream substrates including integrins, cadherins, growth factor receptors, and mucins, affecting their stability and signaling. The enzyme interacts with the UDP-galactose transporter and Golgi matrix proteins, and cooperates with sialyltransferases for terminal glycan structures.
In LoVo cells, B4GALT1 knockout disrupts glycosylation of key adhesion and signaling molecules, impairing integrin-dependent attachment, cadherin-mediated junctions, and growth factor receptor activation. This can alter pathways like epithelial-to-mesenchymal transition (EMT) linked to metastatic dissemination. The polyclonal nature captures diverse loss-of-function phenotypes, providing a comprehensive overview of B4GALT1 dependency in colorectal cancer.
This model supports studies on colorectal cancer metastasis, glycosylation-dependent adhesion, glycan biosynthesis, and drug resistance. Typical assays include western blotting for knockout verification, lectin-based flow cytometry for glycan profiling, cell adhesion and transwell migration/invasion assays for functional analysis, colony formation for clonogenicity, and RNA-seq for transcriptomic changes. This product also enables modeling of congenital disorders of glycosylation type IId. For further details, please contact Ascent Research.
