The CCL7 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human SK-HEP-1 liver adenocarcinoma cell line. This product harbors a targeted disruption of the CCL7 gene, generating a loss-of-function model for studying CCL7-dependent processes. The polyclonal nature of the knockout pool reflects a heterogeneous ensemble of CCL7-disrupted alleles, avoiding clonal artifacts and enabling robust functional interrogation in a population context.
The host cell line, SK-HEP-1, was originally established from the ascites of a patient with liver adenocarcinoma and serves as a widely utilized epithelial model for hepatic cancer research. SK-HEP-1 cells display characteristics of malignant hepatocytes and are frequently employed to investigate hepatocellular carcinoma biology, drug responses, and tumor?Cstromal interactions. Their human origin and reproducible growth properties make them a versatile platform for dissecting molecular mechanisms in liver malignancy.
CCL7 encodes the chemokine (C-C motif) ligand 7, a potent chemoattractant for monocytes, T lymphocytes, and eosinophils. This cytokine engages the receptors CCR1, CCR2, and CCR3, triggering downstream intracellular cascades that include G-protein-mediated activation of MAPK/ERK and PI3K-Akt pathways, as well as calcium mobilization and actin polymerization. CCL7 expression is transcriptionally regulated by NF-??B in response to upstream stimuli such as TNF-??, IL-1??, IFN-??, and LPS, placing it at the intersection of inflammatory and chemokine signaling networks.
In the context of the SK-HEP-1 hepatic cancer model, disruption of CCL7 is particularly relevant for examining how tumor-derived chemokines shape the immune microenvironment. SK-HEP-1 cells are known to produce chemotactic factors that recruit monocytes and other leukocytes, potentially influencing tumor progression and immune evasion. The loss of CCL7 function in this cell line may impair the chemotactic signaling that drives directional migration of immune cells toward malignant hepatocytes, thus providing a tractable system to assess the contribution of CCL7 to paracrine crosstalk between tumor cells and the inflammatory milieu.
Researchers can employ this knockout model in a variety of experimental workflows, including western blotting and RT?qPCR to confirm gene disruption and downstream pathway alterations, chemotaxis assays and migration assays to quantify functional outcomes, ELISA and flow cytometry to monitor cytokine production and receptor expression, and co?culture systems with primary immune cells to recapitulate tumor?immune interactions. These applications support investigations into CCL7??s role in liver cancer?associated inflammation, validation of CCL7 as a therapeutic target, and dissection of chemokine?dependent signaling in hepatic malignancies. For further details, please contact Ascent Research.
