DSG2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DSG2 gene has been disrupted. Derived from the SK?HEP?1 liver adenocarcinoma cell line, this loss?of?function model consists of a heterogeneous pool of cells suitable for studying desmoglein?2 biology without clonal selection.
SK?HEP?1 is an adherent human cell line established from the ascites of a patient with liver adenocarcinoma. It displays a mixed epithelial?mesenchymal phenotype and is widely used as a model for hepatic cancer and endothelial biology, making it a competent background for examining adhesion?dependent processes.
Desmoglein?2 (DSG2) is a transmembrane desmosomal cadherin that forms adhesive complexes with plakoglobin, plakophilin?2, desmoplakin, and desmocollin?2. It anchors intermediate filaments and regulates intracellular signaling. DSG2 inhibits Wnt/beta?catenin signaling by sequestering beta?catenin at junctions; its loss releases beta?catenin to activate c?Myc and cyclin D1 transcription. DSG2 is proteolytically cleaved by ADAM17 and MMP9, releasing a soluble ectodomain that influences cell behavior. Downstream mediators include p38 MAPK and Akt, linking desmosome status to proliferation, survival, and motility.
In SK?HEP?1 cells, DSG2 knockout impairs desmosome assembly, reducing intercellular adhesion and promoting epithelial?mesenchymal transition (EMT). The resultant loss of contact inhibition enhances migratory and invasive traits, mirroring events in cancer metastasis. The basal plasticity of SK?HEP?1 cells accentuates these phenotypic shifts, offering a robust system to interrogate desmosome?mediated tumor suppression and cadherin switching.
This polyclonal knockout population is applicable to assays such as western blotting, qPCR, immunofluorescence, migration/invasion assays, TEER, apoptosis assays, co?IP, and phospho?kinase arrays. It supports research into desmosomal dysfunction in hepatic cancer, arrhythmogenic right ventricular cardiomyopathy, pemphigus, and skin fragility. Typical experiments include monitoring beta?catenin localization, quantifying MMP9 secretion, or profiling Akt/p38 MAPK activation. For custom inquiries, contact Ascent Research.
