The HDGF Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, engineered to disrupt the endogenous HDGF (hepatoma-derived growth factor) gene. This product provides a heterogeneous pool of cells carrying targeted gene disruption, generated without single-cell cloning. The polyclonal format is well-suited for experiments requiring a genetically diverse knockout background, enabling robust assessment of HDGF functional roles without clonal selection bias.
The parental HeLa cell line is a widely studied immortalized human epithelial cell line derived from cervical adenocarcinoma tissue and harbors integrated human papillomavirus type 18 (HPV18) sequences. These cells serve as a classic model for cervical cancer research and are extensively used in cancer biology, signal transduction, and drug screening studies. HeLa cells exhibit rapid proliferation and are permissive to a variety of genetic manipulations, making them a reliable host for knockout studies.
HDGF encodes a heparin-binding growth factor that functions as a secreted mitogen and angiogenic factor. Upon secretion, HDGF binds to cell-surface nucleolin, facilitating internalization and triggering the MAPK/ERK and PI3K/AKT cascades. This signaling promotes cell proliferation, migration, and angiogenesis while suppressing apoptosis through transcriptional upregulation of targets such as Cyclin D1, VEGF, MMP-2, MMP-9, Bcl-2, and c-Myc. HDGF activity is modulated by upstream regulators including EGF, hypoxia, SP1, NF-??B, and TGF-??1, and it interacts with nucleolin and CRM1/exportin-1. Additionally, HDGF enhances ??-catenin transcriptional activity via the Wnt pathway, linking it to multiple oncogenic networks.
In the context of cervical adenocarcinoma, HDGF overexpression has been correlated with tumor progression, metastasis, and poor prognosis. The HeLa cell line, originating from cervical cancer, thus provides a pertinent cellular background for investigating HDGF-driven oncogenic mechanisms. Disruption of HDGF in this polyclonal model enables the dissection of its contributions to cancer hallmarks such as sustained proliferation, resistance to apoptosis, and increased migratory capacity, offering a relevant platform for target validation and therapeutic discovery.
Typical applications include validation of HDGF oncogenic function via proliferation assays (MTT/BrdU), migration and invasion transwell assays, and apoptosis analysis (Annexin V/PI). The cells are suitable for screening HDGF inhibitors, exploring tumor angiogenesis by VEGF secretion ELISA, and dissecting HDGF signaling pathways through phospho-ERK and phospho-AKT analyses. Additional uses encompass RT-qPCR and western blotting for gene expression profiling, as well as in vivo tumorigenicity studies. This polyclonal knockout population is intended for research use only. For further information, custom projects, or technical support, please contact Ascent Research.