The ATRN Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatic adenocarcinoma cell line SK-HEP-1, engineered to disrupt the ATRN gene encoding the attractin protein. This loss-of-function model facilitates investigation of attractin’s roles in immune cell adhesion, monocyte-T cell interactions, and melanocortin receptor modulation. The polyclonal format provides a heterogeneous knockout population, mimicking the genetic heterogeneity of tumors and enabling robust functional studies without producing a clonal isolate.
The SK-HEP-1 parental cell line originates from the ascites of a patient with hepatic adenocarcinoma and is extensively characterized as a model for liver cancer research. These adherent epithelial cells exhibit tumorigenic properties in vivo and maintain key signaling pathways relevant to hepatocarcinogenesis. Their use in oncology studies includes investigations of metastasis, drug resistance, and tumor-immune interactions, making them an ideal host for examining ATRN knockout effects.
Attractin is a transmembrane protein that functions upstream of cAMP signaling and interacts with melanocortin receptor MC1R, agouti signaling protein (ASIP), and attractin-like protein ATRNL1. Through these interactions, attractin regulates melanogenesis pathway components such as PKA, MITF, and TYR, as well as T cell activation mediators including TCR/CD3, ZAP70, and NFAT. Upstream stimulation by cytokines and immune activation signals triggers attractin-mediated immune synapse formation and cytokine production. Disruption of ATRN eliminates attractin, thereby perturbing these signaling networks.
In SK-HEP-1 hepatic adenocarcinoma cells, ATRN knockout disrupts potential attractin-dependent modulation of the tumor microenvironment, particularly affecting immune cell clustering and adhesion mechanisms that may influence cancer progression. Although these cells are non-melanocytic, the crossover between attractin-regulated cAMP/PKA signaling and cell proliferation pathways provides a unique system to dissect ATRN’s non-canonical roles in liver cancer. This model helps clarify how attractin loss alters immune evasion and intracellular signaling in a cancerous epithelial context.
This knockout cell product is applicable to a range of research investigations, including functional analysis of ATRN in liver cancer biology, study of immune-tumor cell interactions via adhesion assays, and drug screening targeting attractin-related pathways. Representative experimental techniques include RT-qPCR for ATRN mRNA quantification, Western blot for attractin protein detection, immunofluorescence for subcellular localization, migration and proliferation assays, immune cell adhesion assays, cAMP measurement, and flow cytometry for surface marker profiling. For further information, please contact Ascent Research.
