The IGF2 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human TE1 esophageal squamous cell carcinoma line. This heterogeneous pool of gene-disrupted cells avoids clonal selection artifacts, enabling population-level analyses of IGF2-dependent phenotypes. Each lot is validated to ensure consistent reduction of IGF2 expression across the polyclonal cell pool.
The TE1 cell line was established from a well-differentiated human esophageal squamous cell carcinoma and is widely employed as a model for esophageal cancer research. These epithelial cancer cells exhibit dysregulated growth factor signaling and retain key oncogenic characteristics, making them a relevant platform for investigating molecular mechanisms of carcinogenesis, drug responses, and tumor biology.
IGF2 encodes a mitogenic growth factor that promotes cell proliferation and survival by binding to IGF1R and the insulin receptor isoform A (INSR-A). This activates intracellular signaling through adaptor proteins IRS1 and IRS2, triggering the PI3K/AKT/mTOR and RAS/RAF/MEK/ERK cascades, which upregulate targets such as CCND1, MYC, and BCL2. IGF2 expression is controlled by epigenetic imprinting at the H19/IGF2 locus, transcription factors E2F1 and WT1, and upstream hedgehog and growth hormone signaling, while its bioavailability is modulated by binding proteins IGFBP3 and IGFBP6.
In the TE1 esophageal cancer context, IGF2-driven signaling sustains malignant phenotypes through constitutive activation of AKT1, mTOR, and ERK1/2. Disruption of IGF2 is anticipated to attenuate these pathways, reducing proliferative drive, survival signals, and tumorigenic capacity. This knockout model enables direct investigation of IGF2 contributions to esophageal tumorigenesis, apoptosis resistance, and metastatic potential, as well as studies of imprinting-dependent regulation.
The IGF2 Knockout TE1 Polyclonal Cells support diverse research applications, including functional validation of IGF2 in esophageal cancer, drug target screening for IGF1R/IR inhibitors, and detailed signaling analyses. Representative assays include western blotting for total and phosphorylated AKT and ERK, RT-qPCR for IGF2 mRNA, cell proliferation and colony formation assays, migration and invasion analyses, phospho-signaling profiling, RNA-seq for transcriptomic changes, and xenograft tumor growth models. For further information or to discuss customized experiments, please contact Ascent Research.
