This product is a polyclonal population of CRISPR/Cas9-edited CD47 knockout SK-HEP-1 cells, a human hepatocellular carcinoma cell line. The knockout model is generated through CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of cells with loss-of-function mutations in the CD47 gene. These polyclonal cells provide a versatile tool for studying CD47 biology without the constraints of clonal variation, enabling robust functional assays in a disease-relevant hepatic cancer background. The elimination of CD47 expression disrupts critical immune evasion and cell adhesion mechanisms.
SK-HEP-1 is an epithelial cell line derived from the ascites of a patient with liver adenocarcinoma. It is widely used in liver cancer research due to its well-characterized genomic and phenotypic features, including activation of oncogenic pathways. The cells exhibit a cobblestone-like morphology and retain tumorigenic potential, making them an appropriate host for generating knockout models to investigate molecular drivers of hepatocellular carcinoma.
CD47 encodes an integrin-associated protein that functions as a cell surface receptor for thrombospondin-1 and the inhibitory immune receptor SIRP??. Binding to SIRP?? on macrophages recruits and activates the tyrosine phosphatases SHP-1 and SHP-2, thereby transmitting an anti-phagocytic signal that enables tumor cells to evade innate immune clearance. CD47 expression is regulated by HIF1??, TNF-??, and NF-??B, all of which are frequently elevated in the tumor microenvironment. Moreover, CD47 engages integrins such as ??v??3 and interacts with VEGFR2, linking it to cell adhesion, migration, and survival pathways through FAK and PI3K/Akt signaling. This positions CD47 as a key node in the CD47-SIRP?? immune checkpoint, integrin signaling, and phagocytosis pathways.
In SK-HEP-1 hepatocellular carcinoma cells, CD47-mediated ??don??t eat me?? signaling protects against macrophage-dependent phagocytosis. Knockout of CD47 abrogates this SIRP??-SHP-1/2 axis, potentially enhancing tumor cell susceptibility to immune clearance. Additionally, loss of CD47 may impair integrin-dependent adhesion and FAK/PI3K/Akt signaling, influencing cell migration and metastatic potential. Thus, this knockout model enables dissection of the dual roles of CD47 in immune evasion and cell-matrix interactions in a liver cancer context.
This polyclonal CD47 knockout SK-HEP-1 cell population is suited for functional phagocytosis assays using macrophage co-culture, and for flow cytometric analysis of CD47 expression loss. It supports western blotting studies of SHP-1, phospho-Akt, and FAK, as well as cell adhesion and immunofluorescence assays to assess integrin-mediated interactions. Xenograft tumor models allow evaluation of anti-CD47 therapies. This model advances hepatocellular carcinoma immunotherapy research and CD47-SIRP?? checkpoint inhibitor development. For further details, please contact Ascent Research.
