The JUND Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the JUND gene in the human SK-HEP-1 cell line. This polyclonal format provides a heterogeneous loss-of-function model for studying JUND-dependent transcriptional regulation, enabling investigation of AP-1-mediated gene expression with population-level averaging of knockout effects.
SK-HEP-1 is a human hepatic adenocarcinoma cell line originally established from ascites of a patient with liver adenocarcinoma. These epithelial tumor cells serve as a well-characterized in vitro model for hepatocellular carcinoma (HCC), exhibiting anchorage-independent growth and tumorigenic potential in xenografts. Their relevance to liver cancer biology makes them an ideal host for studying transcription factor function in oncogenic signaling.
JUND is a basic leucine zipper (bZIP) transcription factor of the AP-1 family that forms homodimers or heterodimers with other AP-1 members, including JUN, FOS, FOSB, FOSL1, FOSL2, ATF2, and CREB, to regulate gene expression. Its activity is modulated by upstream kinases such as JNK (MAPK8/9), ERK (MAPK1/3), and p38 MAPK, which are activated by growth factor receptors (e.g., EGFR) and TNF-alpha. JUND binds AP-1 response elements to control transcription of downstream targets such as CCND1 (Cyclin D1), CDKN1A (p21), JUN, FOS, MMP9, and BCL2L11 (BIM), thereby integrating mitogenic and stress signals to influence cell proliferation, apoptosis, and differentiation.
In the SK-HEP-1 hepatocellular carcinoma model, JUND knockout disrupts AP-1-mediated transcriptional programs, affecting cell cycle progression through CCND1 and apoptotic regulation via BCL2L11. This loss-of-function system enables dissection of JUND’s specific contributions to JNK/ERK-driven oncogenic signaling, providing insights into tumor growth, metastasis, and therapeutic responses relevant to liver cancer.
Applications include AP-1 signaling research, liver cancer biology, transcription factor functional analysis, and cancer cell proliferation/apoptosis studies. Representative assays include Western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, immunofluorescence, flow cytometry, migration/invasion assays, AP-1 luciferase reporter assays, phospho-JNK detection, and drug sensitivity testing. The polyclonal population allows for robust phenotypic assessment. For further information, please contact Ascent Research.
