The CAV2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population featuring targeted disruption of the human CAV2 gene. This heterogeneous pool, derived from a bulk selection rather than single-cell clones, provides a robust loss-of-function model that averages editing-induced variability, making it suitable for studies demanding population-level knockout effects. It is supplied as a ready-to-use cell population for diverse downstream assays.
The SK-HEP-1 cell line is a human liver adenocarcinoma model established from ascites, distinguished by its endothelial-like features including expression of certain vascular markers. This dual phenotype makes it an invaluable tool for investigating hepatocellular carcinoma biology alongside endothelial functions such as angiogenesis, transcytosis, and shear stress responses. The adherent, tumor-derived cell line is widely employed in cancer migration, invasion, and drug transport research.
CAV2 encodes caveolin-2, a conserved coat protein that hetero-oligomerizes with CAV1 and the cavin protein PTRF/Cavin-1 to form caveolae, small invaginations of the plasma membrane. These structures serve as signaling platforms by scaffolding a variety of receptors and downstream effectors. CAV2 directly interacts with epidermal growth factor receptor (EGFR), transforming growth factor-?? receptor 1 (TGFBR1), and the insulin receptor (INSR), and helps recruit and regulate effectors including endothelial nitric oxide synthase (eNOS), Src kinase, ERK1/2, AKT, and ??-catenin. Transcriptionally, CAV2 is controlled by EGR-1 and FOXO1, and its expression is induced by TGF-??1, insulin, and EGF. Through these interactions, caveolin-2 modulates caveolae-mediated endocytosis, signal transduction amplitude, and cholesterol homeostasis, ultimately influencing cell proliferation, migration, and differentiation.
Disruption of CAV2 in SK-HEP-1 cells compromises caveolar integrity and the delicate balance of associated signaling networks, providing a potent model to dissect caveolin-2??s role in hepatic cancer progression. The endothelial-like character of SK-HEP-1 further enables detailed studies of CAV2 in vascular biology, including eNOS-dependent vasoregulation and mechanosignaling. The polyclonal knockout approach recapitulates the genetic heterogeneity found in tumors, allowing investigation of how CAV2 loss affects cellular behaviors such as growth factor sensitivity, invasive capacity, and drug resistance.
This polyclonal product supports a broad range of experimental paradigms. Standard validation uses Western blotting for CAV2 and CAV1 protein levels, RT-qPCR for mRNA quantification, and immunofluorescence to visualize caveolar disruption. Co-immunoprecipitation confirms CAV1?CCAV2 complex ablation. Functional assays such as scratch wound healing, Matrigel invasion, and MTT proliferation directly assess migration, invasion, and viability. Flow cytometry enables cell cycle analysis, while phospho-kinase arrays reveal alterations in the activation states of key pathways (e.g., ERK1/2, AKT, Src). For additional information, please reach out to Ascent Research.
