The IGF2BP3 Knockout TE1 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human TE1 esophageal squamous cell carcinoma line. This genetically heterogeneous loss-of-function model enables robust functional studies of IGF2BP3 without requiring single-cell cloning.
The host TE1 cell line was established from a well-differentiated human esophageal squamous cell carcinoma, retaining malignant epithelial characteristics and high proliferative capacity. As an adherent cancerous cell line, TE1 serves as a widely accepted in vitro model for esophageal cancer research, faithfully recapitulating key oncogenic features of the disease.
IGF2BP3 is an RNA-binding protein that selectively recognizes N6-methyladenosine (m6A)-modified mRNAs, stabilizing oncogenic transcripts such as CD44, c-Myc, IGF2, Cyclin D1, and MMP2, thereby enhancing their translation and promoting cell proliferation and migration. Upstream regulators including MYC, LIN28B, and HIF1A drive its expression, while interaction partners like ELAVL1, YBX1, LIN28A, and CNOT1 modulate its activity. Functionally, IGF2BP3 operates downstream of PI3K/AKT signaling through PIK3CA and AKT1 and contributes to Wnt/??-catenin signaling via CTNNB1 and TCF7L2, embedding m6A epitranscriptomic regulation (marked by METTL3) within these oncogenic pathways.
CRISPR/Cas9-mediated disruption of IGF2BP3 in TE1 cells leads to reduced stabilization of its target mRNAs, resulting in attenuated proliferation and migration. This recapitulates the clinically observed association between IGF2BP3 overexpression and poor prognosis in esophageal squamous cell carcinoma and other cancers. The polyclonal knockout population provides a representative sampling of gene disruption events, making it a robust tool for dissecting IGF2BP3-dependent tumorigenic mechanisms in a disease-relevant background.
Key applications encompass post-transcriptional gene regulation, m6A epitranscriptomics, esophageal cancer biology, and drug target validation. Typical downstream assays include Western blotting and RT-qPCR for expression analysis, cell proliferation and migration assays, RNA immunoprecipitation (RIP) and m6A RIP to assess RNA-protein interactions, immunofluorescence, colony formation, and xenograft tumor growth studies. For further details, please contact Ascent Research.
