The E2F4 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the E2F4 gene in the HGC-27 human gastric carcinoma cell line. This polyclonal knockout model provides a powerful tool for loss-of-function studies, enabling investigation of E2F4-dependent regulatory networks in a gastric cancer context. The cells are supplied as a heterogeneous pool following CRISPR/Cas9-mediated gene disruption, retaining the diverse genetic backgrounds typical of polyclonal populations, which is advantageous for studying population-level effects and minimizing clonal artifacts.
The host cell line, HGC-27, is a widely utilized human gastric carcinoma line derived from lymph node metastasis. As an epithelial cancer cell line, HGC-27 retains key molecular characteristics of gastric adenocarcinoma and is commonly employed in research on tumor cell proliferation, invasion, and drug response. Its metastatic origin renders it particularly relevant for studying advanced disease mechanisms, making it a suitable platform for interrogating the roles of cell cycle regulators such as E2F4 in gastric cancer progression.
E2F4 encodes a transcription factor that primarily functions as a repressor of cell cycle genes, maintaining quiescence and driving differentiation. It forms repressive complexes with the pocket proteins pRB, p130, and p107, and recruits chromatin modifiers such as HDAC1 and BRG1 to silence E2F target promoters. E2F4 activity is regulated by upstream signals including CDK4/6-cyclin D1-mediated phosphorylation of pocket proteins, and it integrates inputs from TGF-?? and Wnt signaling pathways. Key downstream targets repressed by E2F4 include cyclin E1 (CCNE1), cyclin A2 (CCNA2), CDC6, MCM2, and MYC, which are critical for G1/S transition and DNA replication. The E2F4-DP1/DP2 heterodimer thus acts as a central node in the pRB/E2F pathway, coordinating cell cycle exit and entry.
Disruption of E2F4 in HGC-27 cells relieves transcriptional repression of cell cycle genes, potentially promoting unchecked proliferation and enhancing tumorigenic properties. This knockout model allows for the dissection of E2F4??s role in gastric cancer, where its dysregulation has been implicated in cell cycle dyscontrol and malignant transformation. In the context of gastric carcinoma, loss of E2F4-mediated repression may alter sensitivity to TGF-?? growth-inhibitory signals or Wnt-driven proliferation, providing insight into how these pathways crosstalk to drive tumor aggressiveness. This polyclonal population is particularly suited for studying heterogeneous responses and identifying E2F4-dependent vulnerabilities.
Typical applications include functional genomics studies to characterize E2F4-regulated transcriptional programs via RNA-seq and ChIP-qPCR, as well as phenotypic analyses measuring cell proliferation (MTT/BrdU), cell cycle distribution, and apoptosis by flow cytometry. Additionally, these cells can be used to assess E2F4??s impact on migration and invasion, and to evaluate drug sensitivity in gastric cancer models. By combining this knockout system with any existing HGC-27 wild-type controls, researchers can precisely define E2F4??s contributions to cancer cell behavior. For further details or customized solutions, please contact Ascent Research.
