The E2F4 Knockout SK-HEP-1 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatic adenocarcinoma line, engineered for targeted disruption of the E2F4 gene. This polyclonal format provides a diverse set of edited alleles, minimizing clonal selection bias and offering a robust model for functional genomics studies in hepatocellular carcinoma research.
SK-HEP-1 is an epithelial cell line isolated from ascites of a liver adenocarcinoma patient, widely adopted as a hepatocellular carcinoma model. These cells exhibit hepatic tumorigenic properties, including anchorage-independent growth and invasive capacity, making them an appropriate host for investigating cell cycle dysregulation and tumor suppressor pathways.
E2F4 encodes a transcriptional repressor that, together with DP transcription factors (TFDP1, TFDP2) and pocket proteins (RB1, RBL1/p107, RBL2/p130), binds E2F promoter elements to silence cell cycle genes such as CCNA2, CCNE1, CDK1, and MYB, as well as the anti-apoptotic factor BIRC5. Repressor activity is relieved by CDK4/6?CCyclin D1-dependent phosphorylation of pocket proteins and is modulated by TGF-?? signaling through direct interaction with SMAD3. Negative regulators p15INK4b and p16INK4a further tune this pathway. Thus, E2F4 integrates growth inhibitory cues to block G1/S transition and promote differentiation.
Disruption of E2F4 in SK-HEP-1 cells likely derepresses S-phase genes, accelerating cell cycle entry and altering proliferative control. This knockout model allows investigation of E2F4’s tumor-suppressive role in liver cancer and its interplay with the pRb-E2F axis and TGF-?? pathways, providing insights into hepatocellular carcinoma progression and potential therapeutic targets.
Typical applications include transcriptomic and proteomic profiling (RNA-seq, RT-qPCR, Western blotting), chromatin occupancy analysis (ChIP-qPCR), cell cycle assessment (flow cytometry with PI staining, BrdU incorporation), proliferation and migration assays (MTT, scratch assay), E2F luciferase reporter assays, and apoptosis detection. These tools support mechanism-of-action studies, drug screening targeting cell cycle regulators, and TGF-?? signaling research. For inquiries or custom applications, please contact Ascent Research.
