The DUSP23 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatocellular carcinoma SK-HEP-1 cell line. This product contains a heterogeneous pool of cells with targeted disruptions in the DUSP23 gene, enabling loss-of-function studies without clonal isolation. The polyclonal format offers a cost-effective and rapid path to interrogate DUSP23 function in a liver cancer context, suitable for bulk population assays.
SK-HEP-1 is an epithelial cell line originally established from the ascites of a patient with liver adenocarcinoma. It is a well-established model for hepatocellular carcinoma research, exhibiting properties relevant to hepatic tumor biology such as metabolic alterations, invasive capacity, and drug sensitivity. The cell line’s genetic tractability makes it suitable for CRISPR-based gene editing.
DUSP23 is a dual-specificity phosphatase that negatively regulates stress-activated MAP kinase pathways by dephosphorylating p38?? (MAPK14) and JNK isoforms (MAPK8, MAPK9, MAPK10). It is activated by diverse cellular stresses and cytokines, including TNF-?? and IL-1??, and acts downstream of MAP3Ks like ASK1, MEKK1, and TAK1. DUSP23 directly interacts with these MAPKs to attenuate signaling, thereby controlling the phosphorylation of downstream factors such as ATF2, c-Jun, and MAPKAPK2. Through this activity, DUSP23 modulates cell proliferation, survival, and differentiation in response to environmental cues.
In hepatocellular carcinoma, aberrant MAPK signaling contributes to tumor development and progression. Knockout of DUSP23 in SK-HEP-1 cells results in sustained activation of p38 and JNK, potentially enhancing proliferative, survival, and stress-adaptive responses. This model is therefore instrumental for dissecting the tumor-suppressive or oncogenic functions of DUSP23, clarifying its role in liver cancer pathogenesis and therapeutic responses.
Research applications include detailed signaling studies using Western blotting for phospho-p38 and phospho-JNK, RT-qPCR for DUSP23 and downstream targets, and functional assays such as MTT proliferation, wound healing migration, and apoptosis (Annexin V/PI). Transcriptome profiling via RNA-seq can identify broader regulatory networks affected by DUSP23 loss. These cells are suitable for functional genomics and drug sensitivity screening in hepatocellular carcinoma. For further information, contact Ascent Research.
